cholecalciferol and Body-Weight

Middle East Respiratory Syndrome (MERS) is a novel respiratory illness firstly reported in Saudi Arabia in 2012. It is caused by a new corona virus, called MERS corona virus (MERS-CoV). Most people who have MERS-CoV infection developed severe acute respiratory illness.. This work is done to determine the clinical characteristics and the outcome of intensive care unit (ICU) admitted patients with confirmed MERS-CoV infection.. This study included 32 laboratory confirmed MERS corona virus infected patients who were admitted into ICU. It included 20 (62.50%) males and 12 (37.50%) females. The mean age was 43.99 ± 13.03 years. Diagnosis was done by real-time reverse transcription polymerase chain reaction (rRT-PCR) test for corona virus on throat swab, sputum, tracheal aspirate, or bronchoalveolar lavage specimens. Clinical characteristics, co-morbidities and outcome were reported for all subjects.. Most MERS corona patients present with fever, cough, dyspnea, sore throat, runny nose and sputum. The presence of abdominal symptoms may indicate bad prognosis. Prolonged duration of symptoms before patients' hospitalization, prolonged duration of mechanical ventilation and hospital stay, bilateral radiological pulmonary infiltrates, and hypoxemic respiratory failure were found to be strong predictors of mortality in such patients. Also, old age, current smoking, smoking severity, presence of associated co-morbidities like obesity, diabetes mellitus, chronic heart diseases, COPD, malignancy, renal failure, renal transplantation and liver cirrhosis are associated with a poor outcome of ICU admitted MERS corona virus infected patients.. Plasma HO-1, ferritin, p21, and NQO1 were all elevated at baseline in CKD participants. Plasma HO-1 and urine NQO1 levels each inversely correlated with eGFR (. SnPP can be safely administered and, after its injection, the resulting changes in plasma HO-1, NQO1, ferritin, and p21 concentrations can provide information as to antioxidant gene responsiveness/reserves in subjects with and without kidney disease.. A Study with RBT-1, in Healthy Volunteers and Subjects with Stage 3-4 Chronic Kidney Disease, NCT0363002 and NCT03893799.. HFNC did not significantly modify work of breathing in healthy subjects. However, a significant reduction in the minute volume was achieved, capillary [Formula: see text] remaining constant, which suggests a reduction in dead-space ventilation with flows > 20 L/min. (ClinicalTrials.gov registration NCT02495675).. 3 组患者手术时间、术中显性失血量及术后 1 周血红蛋白下降量比较差异均无统计学意义（. 对于肥胖和超重的膝关节单间室骨关节炎患者，采用 UKA 术后可获满意短中期疗效，远期疗效尚需进一步随访观察。.. Decreased muscle strength was identified at both time points in patients with hEDS/HSD. The evolution of most muscle strength parameters over time did not significantly differ between groups. Future studies should focus on the effectiveness of different types of muscle training strategies in hEDS/HSD patients.. These findings support previous adverse findings of e-cigarette exposure on neurodevelopment in a mouse model and provide substantial evidence of persistent adverse behavioral and neuroimmunological consequences to adult offspring following maternal e-cigarette exposure during pregnancy. https://doi.org/10.1289/EHP6067.. This RCT directly compares a neoadjuvant chemotherapy regimen with a standard CROSS regimen in terms of overall survival for patients with locally advanced ESCC. The results of this RCT will provide an answer for the controversy regarding the survival benefits between the two treatment strategies.. NCT04138212, date of registration: October 24, 2019.. Results of current investigation indicated that milk type and post fermentation cooling patterns had a pronounced effect on antioxidant characteristics, fatty acid profile, lipid oxidation and textural characteristics of yoghurt. Buffalo milk based yoghurt had more fat, protein, higher antioxidant capacity and vitamin content. Antioxidant and sensory characteristics of T. If milk is exposed to excessive amounts of light, Vitamins B. The two concentration of ZnO nanoparticles in the ambient air produced two different outcomes. The lower concentration resulted in significant increases in Zn content of the liver while the higher concentration significantly increased Zn in the lungs (p < 0.05). Additionally, at the lower concentration, Zn content was found to be lower in brain tissue (p < 0.05). Using TEM/EDX we detected ZnO nanoparticles inside the cells in the lungs, kidney and liver. Inhaling ZnO NP at the higher concentration increased the levels of mRNA of the following genes in the lungs: Mt2 (2.56 fold), Slc30a1 (1.52 fold) and Slc30a5 (2.34 fold). At the lower ZnO nanoparticle concentration, only Slc30a7 mRNA levels in the lungs were up (1.74 fold). Thus the two air concentrations of ZnO nanoparticles produced distinct effects on the expression of the Zn-homeostasis related genes.. Until adverse health effects of ZnO nanoparticles deposited in organs such as lungs are further investigated and/or ruled out, the exposure to ZnO nanoparticles in aerosols should be avoided or minimised.

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There is considerable variation in incremental circulating 25-hydroxyvitamin D (25OHD) levels on vitamin D supplements, even when similar age groups and identical vitamin D doses are compared. We therefore aimed to investigate the importance of body weight for the dose-response relation in circulating 25OHD.. We performed a systematic review of randomized placebo-controlled vitamin D supplementation trials in all age groups ≥10 years to clarify the influence of body weight and other parameters on incremental circulating 25OHD levels (difference between baseline and in-study values) in vitamin D-deficient and non-deficient individuals.. We included 144 cohorts from 94 independent studies, published from 1990 to November 2012, in our systematic review. There was a logarithmic association between vitamin D dose per kg body weight per day and increment in circulating 25OHD. In multivariable regression analysis, vitamin D dose per kg body weight per day could explain 34.5% of variation in circulating 25OHD. Additional significant predictors were type of supplement (vitamin D2 or vitamin D3), age, concomitant intake of calcium supplements and baseline 25OHD, explaining 9.8, 3.7, 2.4 and 1.9%, respectively, of the variation in circulating 25OHD.. This systematic review demonstrates that body weight is an important predictor of variation in circulating 25OHD in cohorts on vitamin D supplements. Our model provides an estimate of the daily vitamin D dose that is necessary for achieving adequate circulating 25OHD levels in vitamin D-insufficient or vitamin D-deficient individuals/cohorts with different body weights and ages.

Topics: Adolescent; Adult; Age Factors; Aged; Aged, 80 and over; Body Weight; Calcium; Child; Cholecalciferol; Dietary Supplements; Ergocalciferols; Female; Humans; Male; Middle Aged; Vitamin D; Vitamin D Deficiency

Topics: Animal Feed; Animals; Body Weight; Cattle; Cholecalciferol; Diet; Dietary Supplements; Endotoxins; Lipopolysaccharides; Male; Milk; Vitamins; Weaning

The relationship between maternal and infant vitamin D and early childhood growth remains inadequately understood.. This work aimed to investigate how maternal and child 25-hydroxyvitamin D (25[OH]D) and vitamin D supplementation affect growth during the first 2 years of life.. A randomized, double-blinded, single-center intervention study was conducted from pregnancy until offspring age 2 years. Altogether 812 term-born children with complete data were recruited at a maternity hospital. Children received daily vitamin D3 supplementation of 10 μg (group 10) or 30 μg (group 30) from age 2 weeks to 2 years. Anthropometry and growth rate were measured at age 1 and 2 years.. Toddlers born to mothers with pregnancy 25(OH)D greater than 125 nmol/L were at 2 years lighter and thinner than the reference group with 25(OH)D of 50 to 74.9 nmol/L (P < .010). Mean 2-year 25(OH)D concentrations were 87 nmol/L in group 10 and 118 nmol/L in group 30 (P < .001). When group 30 was compared with group 10, difference in body size was not statistically significant (P > .053), but group 30 had slower growth in length and head circumference between 6 months and 1 year (P < .047), and more rapid growth in weight and length-adjusted weight between 1 and 2 years (P < .043). Toddlers in the highest quartile of 25(OH)D (> 121 nmol/L) were shorter (mean difference 0.2 SD score [SDS], P = .021), lighter (mean difference 0.4 SDS, P = .001), and thinner (in length-adjusted weight) (mean difference 0.4 SDS, P = .003) compared with the lowest quartile (< 81.2 nmol/L).. Vitamin D and early childhood growth may have an inverse U-shaped relationship.

Topics: Adult; Body Size; Body Weight; Child Development; Child, Preschool; Cholecalciferol; Dietary Supplements; Double-Blind Method; Female; Finland; Humans; Infant; Infant, Newborn; Male; Pregnancy; Prenatal Exposure Delayed Effects; Vitamin D; Vitamin D Deficiency

We evaluated the efficacy of muscle-targeted nutritional support on the functional outcomes of multidisciplinary intensive rehabilitation treatment (MIRT) in patients with Parkinson disease (PD) or parkinsonism.. We conducted a pragmatic, bicentric, randomized (1:1), assessor-blind controlled trial (Protein, Leucine and Vitamin D Enhancing Rehabilitation [PRO-LEADER]; April 2017 to January 2018) in cognitively intact patients with PD or parkinsonism and undergoing a 30-day MIRT. Patients (n = 150) received a standard hospital diet with or without a whey protein-based nutritional supplement enriched with leucine and vitamin D twice daily. The primary efficacy endpoint was the increase in the distance walked during a 6-minute walking test (6MWT). Secondary endpoints were changes in 4-meter walking speed, Timed Up and Go test (TUG), Berg balance scale, handgrip strength, Self-assessment Parkinson's Disease Disability Scale, body weight, and skeletal muscle mass (SMM).. Nutritional support resulted in greater increase in the distance walked during 6MWT (mean 69.6 meters [95% confidence interval (CI) 60.7-78.6]) than no support (51.8 meters [95% CI 37.0-66.7]): center-adjusted mean difference, 18.1 meters (95% CI 0.9-35.3) (. The consumption of a whey protein-based nutritional formula enriched with leucine and vitamin D with MIRT improved lower extremity function and preserved muscle mass in patients with PD or parkinsonism.Clinicaltrials.gov IDENTIFIER: NCT03124277.. This study provides Class I evidence that for patients with parkinsonism undergoing intensive rehabilitation, a whey protein-based nutritional formula enriched with leucine and vitamin D increased distance walked on the 6MWT.

Topics: Aged; Amino Acids, Essential; Body Weight; Cholecalciferol; Dietary Proteins; Dietary Supplements; Female; Food, Fortified; Humans; Leucine; Male; Middle Aged; Muscle, Skeletal; Nutritional Support; Parkinson Disease; Parkinsonian Disorders; Physical Functional Performance; Treatment Outcome; Vitamins; Walk Test; Walking Speed; Whey Proteins

Obesity and overweight are associated with vitamin D deficiency and hyperhomocysteinemia, all of which are contributing factors for developing cardiovascular disease (CVD). Therefore, we hypothesized that improving serum 25-hydroxyvitamin D [25(OH)D] levels may decrease the body weight and total homocysteine concentrations among overweight reproductive women. To test our hypothesis, a randomized, double-blind placebo-controlled clinical trial, registered under ClinicalTrials.gov Identifier No. NCT03310307, was conducted on 100 overweight reproductive women that were allocated into two groups, namely, the treatment group (n = 50), which received 50 000 IU vitamin D

Topics: Adult; Body Mass Index; Body Weight; Calcium; Cardiovascular Diseases; Cholecalciferol; Double-Blind Method; Female; Homocysteine; Humans; Obesity; Overweight; Parathyroid Hormone; Phosphorus; Vitamin D; Vitamin D Deficiency; Young Adult

To determine the effects of vitamin D (VD) supplementation and isokinetic training on muscle strength, explosive strength (counter movement jump) (ES), lean body mass (LBM) and gait parameters in severe pediatric burn.. Forty-eight burned children with circumferential lower extremity burns covering 40-55% of the total body surface area (TBSA), aged 10-16 years (Mean±SD 13.01±1.75), were randomized into the standard of care (n=16), isokinetic (n=17) and VD (n=15) groups. Unburned children (n=20) served as matched controls. All burned children received 12 weeks of routine physical therapy program (RPTP). In addition, the isokinetic group received isokinetic training for the quadriceps dominant limb 3 times per week at angular velocity 150°/s, and the VD group received the isokinetic training plus an oral daily dose of vitamin D. The VD and isokinetic groups showed significant improvement in quadriceps strength, ES, LBM and gait parameters compared with the standard of care, and VD group show significant improvement in the VD level as compared with the other groups. The outcome measures (and percent of improvement where applicable) for the VD, isokinetic and standard of care are as follows: quadriceps strength, 85.25±0.93Nm (85%), 64.25±0.93 (36%) and 51.88±1.31Nm (12%); stride length, 94.00±2.69 (7%), 110.60±2.87 (25%) and 139.56±2.57 (60%); step length, 67.26±2.45 (72%), 55.25±2.49 (43%) and 43.76±1.34 (18%); velocity, 133.94±1.65 (82%), 99.94±1.65 (35%) and 80.11±1.91 (9%); and cadence, 140.63±1.36 (68%), 132.63±1.36 (58%) and 90.35±1.32 (9%), VD level 43.33±7.48 (75%), 24.77±7.38 (5%) and 25.63±8.39 (4%) respectively.. VD supplementation combined with exercise training significantly increased muscle strength, ES, LBM, gait and VD level in severely burned children.

Topics: Adolescent; Analysis of Variance; Body Weight; Burns; Case-Control Studies; Child; Cholecalciferol; Dietary Supplements; Exercise Therapy; Female; Gait; Humans; Lower Extremity; Male; Muscle Strength; Muscle, Skeletal; Vitamin D; Vitamins

The effects of higher than recommended vitamin D doses on bone mineral density (BMD) and quality are not known. In this study, higher intakes, in postmenopausal women undergoing weight control over 1 year, had no effect on areal or volumetric BMD but prevented the deterioration in cortical bone geometry.. Studies examining how bone responds to a standard dose of vitamin D supplementation have been inconsistent. In addition, the effects of higher doses on BMD and quality are not known. Postmenopausal women undergoing weight control to improve health outcomes are particularly at risk for bone loss and might benefit from supplemental vitamin D intake above the recommended allowance.. The decline in Ct thickness was prevented with higher vitamin D

Topics: Aged; Anthropometry; Body Composition; Body Weight; Bone Density; Bone Density Conservation Agents; Cholecalciferol; Diet, Reducing; Dietary Supplements; Dose-Response Relationship, Drug; Double-Blind Method; Exercise; Female; Humans; Middle Aged; Obesity; Osteoporosis, Postmenopausal; Postmenopause; Weight Loss

Middle East Respiratory Syndrome (MERS) is a novel respiratory illness firstly reported in Saudi Arabia in 2012. It is caused by a new corona virus, called MERS corona virus (MERS-CoV). Most people who have MERS-CoV infection developed severe acute respiratory illness.. This work is done to determine the clinical characteristics and the outcome of intensive care unit (ICU) admitted patients with confirmed MERS-CoV infection.. This study included 32 laboratory confirmed MERS corona virus infected patients who were admitted into ICU. It included 20 (62.50%) males and 12 (37.50%) females. The mean age was 43.99 ± 13.03 years. Diagnosis was done by real-time reverse transcription polymerase chain reaction (rRT-PCR) test for corona virus on throat swab, sputum, tracheal aspirate, or bronchoalveolar lavage specimens. Clinical characteristics, co-morbidities and outcome were reported for all subjects.. Most MERS corona patients present with fever, cough, dyspnea, sore throat, runny nose and sputum. The presence of abdominal symptoms may indicate bad prognosis. Prolonged duration of symptoms before patients' hospitalization, prolonged duration of mechanical ventilation and hospital stay, bilateral radiological pulmonary infiltrates, and hypoxemic respiratory failure were found to be strong predictors of mortality in such patients. Also, old age, current smoking, smoking severity, presence of associated co-morbidities like obesity, diabetes mellitus, chronic heart diseases, COPD, malignancy, renal failure, renal transplantation and liver cirrhosis are associated with a poor outcome of ICU admitted MERS corona virus infected patients.. Plasma HO-1, ferritin, p21, and NQO1 were all elevated at baseline in CKD participants. Plasma HO-1 and urine NQO1 levels each inversely correlated with eGFR (. SnPP can be safely administered and, after its injection, the resulting changes in plasma HO-1, NQO1, ferritin, and p21 concentrations can provide information as to antioxidant gene responsiveness/reserves in subjects with and without kidney disease.. A Study with RBT-1, in Healthy Volunteers and Subjects with Stage 3-4 Chronic Kidney Disease, NCT0363002 and NCT03893799.. HFNC did not significantly modify work of breathing in healthy subjects. However, a significant reduction in the minute volume was achieved, capillary [Formula: see text] remaining constant, which suggests a reduction in dead-space ventilation with flows > 20 L/min. (ClinicalTrials.gov registration NCT02495675).. 3 组患者手术时间、术中显性失血量及术后 1 周血红蛋白下降量比较差异均无统计学意义（. 对于肥胖和超重的膝关节单间室骨关节炎患者，采用 UKA 术后可获满意短中期疗效，远期疗效尚需进一步随访观察。.. Decreased muscle strength was identified at both time points in patients with hEDS/HSD. The evolution of most muscle strength parameters over time did not significantly differ between groups. Future studies should focus on the effectiveness of different types of muscle training strategies in hEDS/HSD patients.. These findings support previous adverse findings of e-cigarette exposure on neurodevelopment in a mouse model and provide substantial evidence of persistent adverse behavioral and neuroimmunological consequences to adult offspring following maternal e-cigarette exposure during pregnancy. https://doi.org/10.1289/EHP6067.. This RCT directly compares a neoadjuvant chemotherapy regimen with a standard CROSS regimen in terms of overall survival for patients with locally advanced ESCC. The results of this RCT will provide an answer for the controversy regarding the survival benefits between the two treatment strategies.. NCT04138212, date of registration: October 24, 2019.. Results of current investigation indicated that milk type and post fermentation cooling patterns had a pronounced effect on antioxidant characteristics, fatty acid profile, lipid oxidation and textural characteristics of yoghurt. Buffalo milk based yoghurt had more fat, protein, higher antioxidant capacity and vitamin content. Antioxidant and sensory characteristics of T. If milk is exposed to excessive amounts of light, Vitamins B. The two concentration of ZnO nanoparticles in the ambient air produced two different outcomes. The lower concentration resulted in significant increases in Zn content of the liver while the higher concentration significantly increased Zn in the lungs (p < 0.05). Additionally, at the lower concentration, Zn content was found to be lower in brain tissue (p < 0.05). Using TEM/EDX we detected ZnO nanoparticles inside the cells in the lungs, kidney and liver. Inhaling ZnO NP at the higher concentration increased the levels of mRNA of the following genes in the lungs: Mt2 (2.56 fold), Slc30a1 (1.52 fold) and Slc30a5 (2.34 fold). At the lower ZnO nanoparticle concentration, only Slc30a7 mRNA levels in the lungs were up (1.74 fold). Thus the two air concentrations of ZnO nanoparticles produced distinct effects on the expression of the Zn-homeostasis related genes.. Until adverse health effects of ZnO nanoparticles deposited in organs such as lungs are further investigated and/or ruled out, the exposure to ZnO nanoparticles in aerosols should be avoided or minimised.

Topics: A549 Cells; Acetylmuramyl-Alanyl-Isoglutamine; Acinetobacter baumannii; Acute Lung Injury; Adaptor Proteins, Signal Transducing; Adenine; Adenocarcinoma; Adipogenesis; Administration, Cutaneous; Administration, Ophthalmic; Adolescent; Adsorption; Adult; Aeromonas hydrophila; Aerosols; Aged; Aged, 80 and over; Aging; Agriculture; Air Pollutants; Air Pollution; Airway Remodeling; Alanine Transaminase; Albuminuria; Aldehyde Dehydrogenase 1 Family; Algorithms; AlkB Homolog 2, Alpha-Ketoglutarate-Dependent Dioxygenase; Alzheimer Disease; Amino Acid Sequence; Ammonia; Ammonium Compounds; Anaerobiosis; Anesthetics, Dissociative; Anesthetics, Inhalation; Animals; Anti-Bacterial Agents; Anti-HIV Agents; Anti-Infective Agents; Anti-Inflammatory Agents; Antibiotics, Antineoplastic; Antibodies, Antineutrophil Cytoplasmic; Antibodies, Monoclonal, Humanized; Antifungal Agents; Antigens, Bacterial; Antigens, CD; Antigens, Differentiation, Myelomonocytic; Antimetabolites, Antineoplastic; Antineoplastic Agents; Antineoplastic Combined Chemotherapy Protocols; Antioxidants; Antitubercular Agents; Antiviral Agents; Apolipoproteins E; Apoptosis; Arabidopsis; Arabidopsis Proteins; Arsenic; Arthritis, Rheumatoid; Asthma; Atherosclerosis; ATP-Dependent Proteases; Attitude of Health Personnel; Australia; Austria; Autophagy; Axitinib; Bacteria; Bacterial Outer Membrane Proteins; Bacterial Proteins; Bacterial Toxins; Bacterial Typing Techniques; Bariatric Surgery; Base Composition; Bayes Theorem; Benzoxazoles; Benzylamines; beta Catenin; Betacoronavirus; Betula; Binding Sites; Biological Availability; Biological Oxygen Demand Analysis; Biomarkers; Biomarkers, Tumor; Biopsy; Bioreactors; Biosensing Techniques; Birth Weight; Blindness; Blood Chemical Analysis; Blood Gas Analysis; Blood Glucose; Blood Pressure; Blood Pressure Monitoring, Ambulatory; Blood-Brain Barrier; Blotting, Western; Body Mass Index; Body Weight; Bone and Bones; Bone Density; Bone Resorption; Borates; Brain; Brain Infarction; Brain Injuries, Traumatic; Brain Neoplasms; Breakfast; Breast Milk Expression; Breast Neoplasms; Bronchi; Bronchoalveolar Lavage Fluid; Buffaloes; Cadherins; Calcification, Physiologic; Calcium Compounds; Calcium, Dietary; Cannula; Caprolactam; Carbon; Carbon Dioxide; Carboplatin; Carcinogenesis; Carcinoma, Ductal; Carcinoma, Ehrlich Tumor; Carcinoma, Hepatocellular; Carcinoma, Non-Small-Cell Lung; Carcinoma, Pancreatic Ductal; Carcinoma, Renal Cell; Cardiovascular Diseases; Carps; Carrageenan; Case-Control Studies; Catalysis; Catalytic Domain; Cattle; CD8-Positive T-Lymphocytes; Cell Adhesion; Cell Cycle Proteins; Cell Death; Cell Differentiation; Cell Line; Cell Line, Tumor; Cell Movement; Cell Nucleus; Cell Phone Use; Cell Proliferation; Cell Survival; Cell Transformation, Neoplastic; Cell Transformation, Viral; Cells, Cultured; Cellulose; Chemical Phenomena; Chemoradiotherapy; Child; Child Development; Child, Preschool; China; Chitosan; Chlorocebus aethiops; Cholecalciferol; Chromatography, Liquid; Circadian Clocks; Circadian Rhythm; Circular Dichroism; Cisplatin; Citric Acid; Clinical Competence; Clinical Laboratory Techniques; Clinical Trials, Phase I as Topic; Clinical Trials, Phase II as Topic; Clostridioides difficile; Clostridium Infections; Coculture Techniques; Cohort Studies; Cold Temperature; Colitis; Collagen Type I; Collagen Type I, alpha 1 Chain; Collagen Type XI; Color; Connective Tissue Diseases; Copper; Coronary Angiography; Coronavirus 3C Proteases; Coronavirus Infections; Cost of Illness; Counselors; COVID-19; COVID-19 Testing; Creatine Kinase; Creatinine; Cross-Over Studies; Cross-Sectional Studies; Cryoelectron Microscopy; Cryosurgery; Crystallography, X-Ray; Cues; Cultural Competency; Cultural Diversity; Curriculum; Cyclic AMP Response Element-Binding Protein; Cyclin-Dependent Kinase Inhibitor p21; Cycloparaffins; Cysteine Endopeptidases; Cytokines; Cytoplasm; Cytoprotection; Databases, Factual; Denitrification; Deoxycytidine; Diabetes Complications; Diabetes Mellitus; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diagnosis, Differential; Diatoms; Diet; Diet, High-Fat; Dietary Exposure; Diffusion Magnetic Resonance Imaging; Diketopiperazines; Dipeptidyl Peptidase 4; Dipeptidyl-Peptidase IV Inhibitors; Disease Models, Animal; Disease Progression; Disease-Free Survival; DNA; DNA Damage; DNA Glycosylases; DNA Repair; DNA-Binding Proteins; DNA, Bacterial; DNA, Viral; Docetaxel; Dose Fractionation, Radiation; Dose-Response Relationship, Drug; Down-Regulation; Doxorubicin; Drosophila; Drosophila melanogaster; Drug Carriers; Drug Delivery Systems; Drug Liberation; Drug Repositioning; Drug Resistance, Bacterial; Drug Resistance, Multiple, Bacterial; Drug Resistance, Neoplasm; Drug Screening Assays, Antitumor; Drug Synergism; Drug Therapy, Combination; Edema; Edible Grain; Education, Graduate; Education, Medical, Graduate; Education, Pharmacy; Ehlers-Danlos Syndrome; Electron Transport Complex III; Electron Transport Complex IV; Electronic Nicotine Delivery Systems; Emergency Service, Hospital; Empathy; Emulsions; Endothelial Cells; Endurance Training; Energy Intake; Enterovirus A, Human; Environment; Environmental Monitoring; Enzyme Assays; Enzyme Inhibitors; Epithelial Cells; Epithelial-Mesenchymal Transition; Epoxide Hydrolases; Epoxy Compounds; Erythrocyte Count; Erythrocytes; Escherichia coli; Escherichia coli Infections; Escherichia coli Proteins; Esophageal Neoplasms; Esophageal Squamous Cell Carcinoma; Esophagectomy; Estrogens; Etanercept; Ethiopia; Ethnicity; Ethylenes; Exanthema; Exercise; Exercise Test; Exercise Tolerance; Extracellular Matrix; Extracorporeal Membrane Oxygenation; Eye Infections, Fungal; False Negative Reactions; Fatty Acids; Fecal Microbiota Transplantation; Feces; Female; Femur Neck; Fermentation; Ferritins; Fetal Development; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Fibroblasts; Fibroins; Fish Proteins; Flavanones; Flavonoids; Focus Groups; Follow-Up Studies; Food Handling; Food Supply; Food, Formulated; Forced Expiratory Volume; Forests; Fractures, Bone; Fruit and Vegetable Juices; Fusobacteria; G1 Phase Cell Cycle Checkpoints; G2 Phase Cell Cycle Checkpoints; Gamma Rays; Gastrectomy; Gastrointestinal Microbiome; Gastrointestinal Stromal Tumors; Gefitinib; Gels; Gemcitabine; Gene Amplification; Gene Expression; Gene Expression Regulation; Gene Expression Regulation, Bacterial; Gene Expression Regulation, Neoplastic; Gene Expression Regulation, Plant; Gene Knockdown Techniques; Gene-Environment Interaction; Genotype; Germany; Glioma; Glomerular Filtration Rate; Glucagon; Glucocorticoids; Glycemic Control; Glycerol; Glycogen Synthase Kinase 3 beta; Glycolipids; Glycolysis; Goblet Cells; Gram-Negative Bacterial Infections; Granulocyte Colony-Stimulating Factor; Graphite; Greenhouse Effect; Guanidines; Haemophilus influenzae; HCT116 Cells; Health Knowledge, Attitudes, Practice; Health Personnel; Health Services Accessibility; Health Services Needs and Demand; Health Status Disparities; Healthy Volunteers; Heart Failure; Heart Rate; Heart Transplantation; Heart-Assist Devices; HEK293 Cells; Heme; Heme Oxygenase-1; Hemolysis; Hemorrhage; Hepatitis B; Hepatitis B e Antigens; Hepatitis B Surface Antigens; Hepatitis B virus; Hepatitis B, Chronic; Hepatocytes; Hexoses; High-Throughput Nucleotide Sequencing; Hippo Signaling Pathway; Histamine; Histamine Agonists; Histidine; Histone Deacetylase 2; HIV Infections; HIV Reverse Transcriptase; HIV-1; Homebound Persons; Homeodomain Proteins; Homosexuality, Male; Hospice and Palliative Care Nursing; HSP70 Heat-Shock Proteins; Humans; Hyaluronan Receptors; Hydrogen; Hydrogen Peroxide; Hydrogen-Ion Concentration; Hydrolysis; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypoglycemia; Hypoglycemic Agents; Hypoxia; Idiopathic Interstitial Pneumonias; Imaging, Three-Dimensional; Imatinib Mesylate; Immunotherapy; Implementation Science; Incidence; INDEL Mutation; Induced Pluripotent Stem Cells; Industrial Waste; Infant; Infant, Newborn; Inflammation; Inflammation Mediators; Infliximab; Infusions, Intravenous; Inhibitory Concentration 50; Injections; Insecticides; Insulin-Like Growth Factor Binding Protein 5; Insulin-Secreting Cells; Interleukin-1; Interleukin-17; Interleukin-8; Internship and Residency; Intestines; Intracellular Signaling Peptides and Proteins; Ion Transport; Iridaceae; Iridoid Glucosides; Islets of Langerhans Transplantation; Isodon; Isoflurane; Isotopes; Italy; Joint Instability; Ketamine; Kidney; Kidney Failure, Chronic; Kidney Function Tests; Kidney Neoplasms; Kinetics; Klebsiella pneumoniae; Knee Joint; Kruppel-Like Factor 4; Kruppel-Like Transcription Factors; Lactate Dehydrogenase 5; Laparoscopy; Laser Therapy; Lasers, Semiconductor; Lasers, Solid-State; Laurates; Lead; Leukocyte L1 Antigen Complex; Leukocytes, Mononuclear; Light; Lipid Peroxidation; Lipopolysaccharides; Liposomes; Liver; Liver Cirrhosis; Liver Neoplasms; Liver Transplantation; Locomotion; Longitudinal Studies; Lopinavir; Lower Urinary Tract Symptoms; Lubricants; Lung; 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Oocytes; Open Reading Frames; Osteoclasts; Osteogenesis; Osteoporosis; Osteoporosis, Postmenopausal; Outpatients; Ovarian Neoplasms; Ovariectomy; Overweight; Oxazines; Oxidants; Oxidation-Reduction; Oxidative Stress; Oxides; Oxidoreductases; Oxygen; Oxygen Inhalation Therapy; Oxygenators, Membrane; Ozone; Paclitaxel; Paenibacillus; Pain Measurement; Palliative Care; Pancreatic Neoplasms; Pandemics; Parasympathetic Nervous System; Particulate Matter; Pasteurization; Patient Preference; Patient Satisfaction; Pediatric Obesity; Permeability; Peroxiredoxins; Peroxynitrous Acid; Pharmaceutical Services; Pharmacists; Pharmacy; Phaseolus; Phenotype; Phoeniceae; Phosphates; Phosphatidylinositol 3-Kinases; Phospholipid Transfer Proteins; Phospholipids; Phosphorus; Phosphorylation; Photoperiod; Photosynthesis; Phylogeny; Physical Endurance; Physicians; Pilot Projects; Piperidines; Pituitary Adenylate Cyclase-Activating Polypeptide; Plant Extracts; Plant Leaves; Plant Proteins; Plant Roots; Plaque, Atherosclerotic; Pneumonia; Pneumonia, Viral; Point-of-Care Testing; Polyethylene Glycols; Polymers; Polysorbates; Pore Forming Cytotoxic Proteins; Positron Emission Tomography Computed Tomography; Positron-Emission Tomography; Postprandial Period; Poverty; Pre-Exposure Prophylaxis; Prediabetic State; Predictive Value of Tests; Pregnancy; Pregnancy Trimester, First; Pregnancy, High-Risk; Prenatal Exposure Delayed Effects; Pressure; Prevalence; Primary Graft Dysfunction; Primary Health Care; Professional Role; Professionalism; Prognosis; Progression-Free Survival; Prolactin; Promoter Regions, Genetic; Proof of Concept Study; Proportional Hazards Models; Propylene Glycol; Prospective Studies; Prostate; Protein Binding; Protein Biosynthesis; Protein Isoforms; Protein Kinase Inhibitors; Protein Phosphatase 2; Protein Processing, Post-Translational; Protein Serine-Threonine Kinases; Protein Structure, Tertiary; Protein Transport; Proteoglycans; Proteome; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-myc; Proto-Oncogene Proteins c-ret; Proto-Oncogene Proteins p21(ras); Proton Pumps; Protons; Protoporphyrins; Pseudomonas aeruginosa; Pseudomonas fluorescens; Pulmonary Artery; Pulmonary Disease, Chronic Obstructive; Pulmonary Gas Exchange; Pulmonary Veins; Pyrazoles; Pyridines; Pyrimidines; Qualitative Research; Quinoxalines; Rabbits; Random Allocation; Rats; Rats, Sprague-Dawley; Rats, Wistar; Receptors, Histamine H3; Receptors, Immunologic; Receptors, Transferrin; Recombinant Proteins; Recurrence; Reference Values; Referral and Consultation; Regional Blood Flow; Registries; Regulon; Renal Insufficiency, Chronic; Reperfusion Injury; Repressor Proteins; Reproducibility of Results; Republic of Korea; Research Design; Resistance Training; Respiration, Artificial; Respiratory Distress Syndrome; Respiratory Insufficiency; Resuscitation; Retinal Dehydrogenase; Retreatment; Retrospective Studies; Reverse Transcriptase Inhibitors; Rhinitis, Allergic; Ribosomal Proteins; Ribosomes; Risk Assessment; 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STAT3 Transcription Factor; Streptomyces coelicolor; Stress, Psychological; Stroke; Stroke Volume; Structure-Activity Relationship; Students, Medical; Students, Pharmacy; Substance Abuse Treatment Centers; Sulfur Dioxide; Surface Properties; Surface-Active Agents; Surveys and Questionnaires; Survival Analysis; Survival Rate; Survivin; Sweden; Swine; Swine, Miniature; Sympathetic Nervous System; T-Lymphocytes, Regulatory; Talaromyces; Tandem Mass Spectrometry; tau Proteins; Telemedicine; Telomerase; Telomere; Telomere Homeostasis; Temperature; Terminally Ill; Th1 Cells; Thiamethoxam; Thiazoles; Thiophenes; Thioredoxin Reductase 1; Thrombosis; Thulium; Thyroid Cancer, Papillary; Thyroid Carcinoma, Anaplastic; Thyroid Neoplasms; Time Factors; Titanium; Tomography, Emission-Computed, Single-Photon; Tomography, X-Ray Computed; TOR Serine-Threonine Kinases; Transcription Factor AP-1; Transcription Factors; Transcription, Genetic; Transcriptional Activation; Transcriptome; Transforming Growth Factor beta1; 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YAP-Signaling Proteins; Yogurt; Young Adult; Zebrafish; Zebrafish Proteins; Ziziphus

The present study was designed to assess the effects of Ca+vitamin D supplementation on pregnancy outcomes in women with gestational diabetes mellitus (GDM).. A randomized, double-blind, placebo-controlled trial was conducted among sixty women with GDM. Participants were divided into two groups to receive Ca+vitamin D supplements or placebo. Individuals in the Ca+vitamin D group (n 30) received 1000 mg Ca/d and two pearls containing 1250 µg (50 000 IU) of cholecalciferol (vitamin D(3)) during the intervention (one at study baseline and another at day 21 of the intervention); those in the placebo group (n 30) received two placebos of vitamin D at the mentioned times and placebos of Ca every day for 6 weeks. Pregnancy outcomes were determined.. A urban community setting in Arak, Iran.. Sixty women with GDM and their newborns, living in Arak, Iran were enrolled.. Women treated with Ca+vitamin D had a significant decrease in caesarean section rate (23·3 % v. 63·3 %, P=0·002) and maternal hospitalization (0 v. 13·3 %, P=0·03) compared with those receiving placebo. In addition, newborns of GDM women randomized to Ca+vitamin D had no case of macrosomia, while the prevalence of macrosomia among those randomized to placebo was 13·3 % (P=0·03). Lower rates of hyperbilirubinaemia (20·0 % v. 56·7 %, P=0·03) and hospitalization (20·0 % v. 56·7 %, P=0·03) were also seen in the supplemented group of newborns than in the placebo group.. Ca+vitamin D supplementation for 6 weeks among pregnant women with GDM led to decreased caesarean section rate and maternal hospitalization, and decreased macrosomia, hyperbilirubinaemia and hospitalization in newborns.

Topics: Adolescent; Adult; Blood Glucose; Body Mass Index; Body Weight; Calcium, Dietary; Cesarean Section; Cholecalciferol; Diabetes, Gestational; Dietary Supplements; Double-Blind Method; Female; Fetal Macrosomia; Follow-Up Studies; Hospitalization; Humans; Hyperbilirubinemia; Iran; Pregnancy; Pregnancy Complications; Pregnancy Outcome; Vitamin D; Young Adult

The co-existence of vitamin D deficiency with obesity and type 2 diabetes is highly prevalent in the United Arab Emirates. We do not have studies evaluating the vitamin D dose response and sufficiency, and if sufficient substitution dose during a longer period could decrease obesity or change fat distribution in obese type 2 diabetic vitamin D deficient Emiratis.. A randomized double-blind clinical trial was conducted for 6 months followed by another 6 months of un-blinded follow up with 87 obese, type 2 diabetic participants. Serum 25-hydroxy vitamin D (S-25(OH)D), anthropometric data, and life-style factors such as diet and sunlight exposure were measured. The study was executed in 3 phases in two arms vitamin D arm (n = 45) and placebo arm (n = 42); in Phase 1 the vitamin D arm received 6000 IU vitamin D3/day (3 months) followed by Phase 2 with 3000 IU vitamin D3/day. During follow up (phase 3) both the arms were un-blinded and supplemented with 2200 IU vitamin D3/day for another 6 months.. At the baseline a significant (p < 0.01) positive association between body fat mass and body weight (r = 0.97) muscle mass (r = 0.47), water mass (r = 0.54), waist circumference (r = 0.82) and serum PTH (r = 0.28) was observed. On supplementation no significant changes in anthropometric dimensions was observed. S-25(OH) D peaked in phase 1 (77.2 ± 30.1 vs 28.5 ± 9.2, p = 0.003) followed by a decrease in phase 2 (62.3 ± 20.8, p = 0.006) paralleled by a decrease in parathyroid hormone in phase 2 (5.9 ± 2.4 vs 4.5 ± 1.8, p < 0.01) compared to baseline in vitamin D group.. This study shows no significant influence of vitamin D supplementation on weight, fat mass or waist circumference in type 2 diabetic obese vitamin D deficient participants of Arab ethnicity after one year. Despite a relatively high daily dose of vitamin D3 we did not achieve target levels of S-25(OH)D above 75 nmol/L in this population. However, supplementation was safe, improved s- 25 (OH)D also reducing the incidence of eucalcemic parathyroid hormone elevation.. ClinicalTrials.gov Identifier: NCT02101151.

Topics: Adult; Aftercare; Body Composition; Body Weight; Cholecalciferol; Diabetes Mellitus, Type 2; Dietary Supplements; Double-Blind Method; Female; Humans; Male; Middle Aged; Obesity; Parathyroid Hormone; United Arab Emirates; Vitamin D Deficiency; Waist Circumference

Sarcopenia, the loss of skeletal muscle mass, strength, and function, is common in elderly individuals but difficult to treat.. A combination of nutrients was investigated to treat sarcopenia in very frail elderly adults.. We enrolled 38 elderly nursing home residents (11 men and 27 women with a mean ± SD age of 86.6 ± 4.8 y) in a 3-mo randomized, controlled, single-blind, parallel group trial. The participants were randomly allocated to 3 groups. The first group received a daily l-leucine (1.2 g) and cholecalciferol (20 μg)-enriched supplement with 6 g medium-chain triglycerides (TGs) (MCTs) (LD + MCT); the second group received the same leucine and cholecalciferol-enriched supplement with 6 g long-chain TGs (LD + LCT); and the third group did not receive any supplements (control). The supplement and oils were taken at dinner, and changes in muscle mass, strength, and function were monitored.. The increase in body weight in the LD + MCT (1.1 ± 1.0 kg) and LD + LCT (0.8 ± 1.1 kg) groups was greater than that in the control group (-0.5 ± 0.9 kg) (P < 0.05). After 3 mo, participants in the LD + MCT group had a 13.1% increase in right-hand grip strength (1.2 ± 1.0 kg, P < 0.01), a 12.5% increase in walking speed (0.078 ± 0.080 m/s, P < 0.05), a 68.2% increase in a 10-s leg open-and-close test performance (2.31 ± 1.68 n/10 s, P < 0.001), and a 28.2% increase in peak expiratory flow (53 ± 59 L/min, P < 0.01). No significant improvements in muscle mass, strength, or function were observed in the LD + LCT or control groups.. The combined supplementation of MCTs (6 g), leucine-rich amino acids, and cholecalciferol at dinner may improve muscle strength and function in frail elderly individuals. This trial was registered at the University Hospital Medical Information Network Clinical Trials Registry as UMIN000017567.

Topics: Aged, 80 and over; Body Weight; Cholecalciferol; Dietary Supplements; Female; Frail Elderly; Gait; Hand Strength; Humans; Leucine; Male; Muscle Strength; Muscle, Skeletal; Sarcopenia; Single-Blind Method; Triglycerides; Vitamins

The effect of vitamin D supplementation and caloric restriction (CR) on glycemic indices and osteocalcin (OC) is not clear. In this randomized controlled double blind trial, we examined whether vitamin D3 supplementation at 2500 IU/d (D) or placebo has differential effects on markers of insulin sensitivity and bone turnover in overweight/obese postmenopausal women during 6 weeks of caloric restriction (weight loss; WL, n = 39) compared to weight maintenance (WM, n = 37). Seventy-six women (57 ± 6 years) completed this study and the WL groups lost 4 ± 1% of body weight. Baseline serum 25-hydroxyvitamin D (25OHD) was 24.8 ± 5.6 ng/mL at baseline; the rise was greatest in WL-D group (p < 0.05). There was an interaction between vitamin D intake and weight on serum OC, insulin, glucose and markers of insulin sensitivity (p < 0.05). The change in OC was explained by changes in serum 25OHD and insulin (model R(2) = 25.6%). Overall, vitamin D supplementation and CR influence serum osteocalcin levels and modestly favor improvements in insulin sensitivity.

Topics: Aged; Body Weight; Caloric Restriction; Cholecalciferol; Dietary Supplements; Double-Blind Method; Female; Glycemic Index; Humans; Insulin Resistance; Middle Aged; Obesity; Osteocalcin; Overweight; Postmenopause

Supplementation of cholecalciferol 800 IU daily appears to be insufficient to raise vitamin D levels to >75 nmol/l in nursing home (NH) patients.. Our objective was to compare the efficacy of an individualized cholecalciferol loading dose (LD) regimen and a daily dose (DD) regimen of cholecalciferol 800 IU in reaching 25-OH vitamin D (25OHD) levels >75 nmol/l.. A total of 30 NH patients with 25OHD levels <50 nmol/l were included. Patients were randomized using the minimization method in the LD or DD group. The cholecalciferol LD, calculated with an algorithm based on serum 25OHD level and body weight, was administered in divided doses of 50,000 IU twice a week, followed by a monthly maintenance dose of either 50,000 or 25,000 IU. The DD regimen consisted of cholecalciferol 800 IU daily for 26 weeks. Serum 25OHD, calcium, creatinine, phosphate, and parathyroid hormone were measured, and 2-minute walking test, handgrip strength, and timed get up and go test were assessed at baseline (T 0), after 5 weeks (T 5), 12 weeks (T 12), and 26 weeks (T 26). The primary endpoint was the percentage of patients with 25OHD levels >75 nmol/l at T 5. Secondary endpoints were the proportion of patients with 25OHD levels >75 nmol/l at T 26, safety of LD regimen, and improvement of performance tests with normalization of vitamin D levels.. Median baseline 25OHD levels (interquartile range) were comparable between the 14 DD and 16 LD patients: 20.9 (15.9-29.6) and 21.7 (16.4-32.8) nmol/l, respectively. Levels of 25OHD >75 nmol/l at T 5 were reached in 79 % of the 14 LD patients, but in none of the 13 DD patients (p < 0.001). At T 26, 25OHD levels >75 nmol/l were reached in 83 % of the 12 LD patients and in 30 % of the ten DD patients (p < 0.05). Side effects or hypercalcemia were not observed. No improvement of performance tests was observed.. In NH patients with severe 25OHD deficiency, an individualized calculated cholecalciferol LD is likely to be superior to a DD of cholecalciferol 800 IU in terms of the ability to rapidly normalize vitamin D levels.

Topics: Aged; Aged, 80 and over; Algorithms; Body Weight; Cholecalciferol; Dietary Supplements; Endpoint Determination; Female; Hand Strength; Humans; Male; Nursing Homes; Patients; Precision Medicine; Reference Standards; Treatment Outcome; Vitamin D; Vitamin D Deficiency; Vitamins; Walking

This study aimed to investigate the effects of daily intake of vitamin D-fortified yogurt drink (doogh) on central obesity indicators in subjects with type 2 diabetes (T2D) and the possible modulation of this effect by vitamin D receptor (VDR) Cdx-2 genotypes. A total of sixty T2D subjects were randomly allocated to two groups to receive either plain doogh (PD; n 29, containing 170 mg Ca and no vitamin D/250 ml) or vitamin D3-fortified doogh (FD; n 31, containing 170 mg Ca and 12·5 μg/250 ml) twice a day for 12 weeks. 25-hydroxyvitamin D (25(OH)D), glycaemic as well as adiposity indicators were evaluated before and after the intervention. VDR-Cdx-2 genotypes in extended number of T2D subjects in the FD group (n 60) were determined as AA, GA and GG. After 12 weeks, in FD compared with PD, serum 25(OH)D increased (+35·4 v. -4·8 nmol/l; P<0·001) and mean changes of waist circumference (WC; -1·3 v. +1·6 cm; P=0·02), body fat mass (FM; -1·9 v. +0·60 %; P=0·008), truncal fat (TF; -1·1 v. 0·13 %; P=0·003) and visceral adipose tissue (-0·80 v. +0·37 AU; P<0·001) decreased significantly. Circulating 25(OH)D was raised only in the AA group (34·8 nmo/l in AA group v. -6·4 nmol/l in AG and -1·6 nmol/l in GG groups; P<0·001), which was accompanied by a significant decrease in changes of WC (P=0·004), FM% (P=0·01) and TF% (P<0·001) in the AA genotype. Daily intake of vitamin D-FD for 12 weeks improved the central obesity indices in T2D subjects, and the improvement was more pronounced in the carriers of the AA genotype of VDR-Cdx-2.

Topics: Adiposity; Adult; Blood Glucose; Body Mass Index; Body Weight; CDX2 Transcription Factor; Cholecalciferol; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Energy Intake; Female; Food, Fortified; Genotyping Techniques; Homeodomain Proteins; Humans; Male; Middle Aged; Nutrigenomics; Nutrition Assessment; Obesity, Abdominal; Patient Compliance; Polymorphism, Single Nucleotide; Randomized Controlled Trials as Topic; Receptors, Calcitriol; Single-Blind Method; Vitamin D Deficiency; Waist Circumference; Yogurt

Vitamin D deficiency is associated with obesity; whether repletion supports weight loss and changes obesity-related biomarkers is unknown.. We compared 12 mo of vitamin D3 supplementation with placebo on weight, body composition, insulin, and C-reactive protein (CRP) in postmenopausal women in a weight-loss intervention.. A total of 218 overweight/obese women (50-75 y of age) with serum 25-hydroxyvitamin D [25(OH)D] ≥10 ng/mL but <32 ng/mL were randomly assigned to weight loss + 2000 IU oral vitamin D3/d or weight loss + daily placebo. The weight-loss intervention included a reduced-calorie diet (10% weight loss goal) and 225 min/wk of moderate-to-vigorous aerobic activity. Mean 12-mo changes in weight, body composition, serum insulin, CRP, and 25(OH)D were compared between groups (intent-to-treat) by using generalized estimating equations.. A total of 86% of participants completed the 12-mo measurements. The mean (95% CI) change in 25(OH)D was 13.6 (11.6, 15.4) ng/mL in the vitamin D3 arm compared with -1.3 (-2.6, -0.3) ng/mL in the placebo arm (P < 0.0001). Changes in weight [-7.1 (-8.7, -5.7) compared with -7.4 (-8.1, -5.4) kg], body mass index (in kg/m(2): both -2.8), waist circumference [-4.9 (-6.7, -2.9) compared with -4.5 (-5.6, -2.6) cm], percentage body fat [-4.1 (-4.9, -2.9) compared with -3.5 (-4.5, -2.5)], trunk fat [-4.1 (-4.7, -3.0) compared with -3.7 (-4.3, -2.9) kg], insulin [-2.5 (-3.4, -1.7) compared with -2.4 (-3.3, -1.4) μU/mL], and CRP [-0.9 (-1.2, -0.6) compared with -0.79 (-0.9, -0.4) mg/L] [corrected] were similar between groups (all P > 0.05). Compared with women who achieved 25(OH)D <32 ng/mL, women randomly assigned to vitamin D who became replete (ie, 25(OH)D ≥32 ng/mL) lost more weight [-8.8 (-11.1, -6.9) compared with -5.6 (-7.2, -5.0) kg; P = 0.05], waist circumference [-6.6 (-9.3, -4.3) compared with -2.5 (-4.6, -2.0) cm; P = 0.02], and percentage body fat [-4.7 (-6.1, -3.5) compared with -2.6 (-3.9, -2.2); P = 0.04]. Among women with complete pill counts (97% adherence), the mean decrease in CRP was 1.18 mg/mL (46%) in the vitamin D arm compared with 0.46 mg/mL (25%) in the placebo arm (P = 0.03).. Vitamin D3 supplementation during weight loss did not increase weight loss or associated factors compared with placebo; however, women who became replete experienced greater improvements. This trial was registered at clinicaltrials.gov as NCT01240213.

Topics: Aged; Body Composition; Body Mass Index; Body Weight; C-Reactive Protein; Cholecalciferol; Diet; Dietary Supplements; Double-Blind Method; Energy Intake; Exercise; Female; Humans; Insulin; Linear Models; Middle Aged; Obesity; Patient Compliance; Postmenopause; Vitamin D Deficiency; Waist Circumference; Weight Loss

Recent evidence suggests that higher calcium and/or vitamin D intake may be associated with lower body weight and better metabolic health. Due to contradictory findings from intervention trials, we investigated the effect of calcium plus vitamin D3 (calcium+D) supplementation on anthropometric and metabolic profiles during energy restriction in healthy, overweight and obese adults with very-low calcium consumption.. Fifty-three subjects were randomly assigned in an open-label, randomized controlled trial to receive either an energy-restricted diet (-500 kcal/d) supplemented with 600 mg elemental calcium and 125 IU vitamin D3 or energy restriction alone for 12 weeks. Repeated measurements of variance were performed to evaluate the differences between groups for changes in body weight, BMI, body composition, waist circumference, and blood pressures, as well as in plasma TG, TC, HDL, LDL, glucose and insulin concentrations.. Eighty-one percent of participants completed the trial (85% from the calcium + D group; 78% from the control group). A significantly greater decrease in fat mass loss was observed in the calcium + D group (-2.8±1.3 vs.-1.8±1.3 kg; P=0.02) than in the control group, although there was no significant difference in body weight change (P>0.05) between groups. The calcium + D group also exhibited greater decrease in visceral fat mass and visceral fat area (P<0.05 for both). No significant difference was detected for changes in metabolic variables (P>0.05).. Calcium plus vitamin D3 supplementation for 12 weeks augmented body fat and visceral fat loss in very-low calcium consumers during energy restriction.. ClinicalTrials.gov (NCT01447433, http://clinicaltrials.gov/).

Topics: Blood Glucose; Blood Pressure; Body Composition; Body Mass Index; Body Weight; Calcium, Dietary; Cholecalciferol; Cholesterol, HDL; Cholesterol, LDL; Diet, Reducing; Dietary Supplements; Energy Intake; Female; Humans; Insulin; Intra-Abdominal Fat; Male; Obesity; Overweight; Students; Triglycerides; Waist Circumference; Young Adult

The US Surgeon General's Report on Bone Health suggests America's bone-health is in jeopardy and issued a "call to action" to develop bone-health plans incorporating components of (1) improved nutrition, (2) increased health literacy, and (3) increased physical activity.. To conduct a Comparative Effectiveness Research (CER) study comparing changes in bone mineral density in healthy women over-40 with above-average compliance when following one of three bone health Plans incorporating the SG's three components.. Using an open-label sequential design, 414 females over 40 years of age were tested, 176 of whom agreed to participate and follow one of three different bone-health programs. One Plan contained a bone-health supplement with 1,000 IUs of vitamin D(3 )and 750 mg of a plant-sourced form of calcium for one year. The other two Plans contained the same plant form of calcium, but with differing amounts of vitamin D(3) and other added bone health ingredients along with components designed to increase physical activity and health literacy. Each group completed the same baseline and ending DXA bone density scans, 43-chemistry blood test panels, and 84-item Quality of Life Inventory (QOL). Changes for all subjects were annualized as percent change in BMD from baseline. Using self-reports of adherence, subjects were rank-ordered and dichotomized as "compliant" or "partially compliant" based on the median rating. Comparisons were also made between the treatment groups and two theoretical age-adjusted expected groups: a non-intervention group and a group derived from a review of previously published studies on non-plant sources of calcium.. There were no significant differences in baseline BMD between those who volunteered versus those who did not and between those who completed per protocol (PP) and those who were lost to attrition. Among subjects completing per protocol, there were no significant differences between the three groups on baseline measurements of BMD, weight, age, body fat and fat-free mass suggesting that the treatment groups were statistically similar at baseline. In all three treatment groups subjects with above average compliance had significantly greater increases in BMD as compared to the two expected-change reference groups. The group following the most nutritionally comprehensive Plan outperformed the other two groups. For all three groups, there were no statistically significant differences between baseline and ending blood chemistry tests or the QOL self-reports.. The increases in BMD found in all three treatment groups in this CER stand in marked contrast to previous studies reporting that interventions with calcium and vitamin D(3) reduce age-related losses of BMD, but do not increase BMD. Increased compliance resulted in increased BMD levels. No adverse effects were found in the blood chemistry tests, self-reported quality of life and daily tracking reports. The Plans tested suggest a significant improvement over the traditional calcium and vitamin D(3) standard of care.

Topics: Adipose Tissue; Adult; Aged; Aged, 80 and over; Ascorbic Acid; Blood Glucose; Body Weight; Bone Density; Boron; C-Reactive Protein; Calcium; Cholecalciferol; Comparative Effectiveness Research; Dietary Supplements; Female; Humans; Lipids; Magnesium; Middle Aged; Minerals; Motor Activity; Patient Education as Topic; Plant Extracts; Quality of Life; Strontium; Treatment Outcome; Vitamin K 2

In Switzerland, children are prescribed 7.5-12.5 μg per day of vitamin D(3) dissolved in alcohol, but many families do not adhere to the recommendation. The aim of the trial was to compare the acceptance of vitamin D(3) dissolved in alcohol or in medium-chain triglycerides among mothers of Swiss newborn infants. The acceptance was tested in 42 healthy newborn infants (20 girls and 22 boys) aged between 2 and 7 days. Their neonatal body weight ranged between 2.225 and 4.150 kg, and the gestational age between 36 1/7 and 41 3/7 weeks. The blinded mothers rated the facial reaction of their children by pointing on a facial hedonic scale. Thirty eight of the 41 mothers, who brought the comparison to completion, assigned a better score to the oily preparation with no difference in the remaining three cases (P < 0.0001). The acceptance for the oily preparation was significantly better both among mothers whose babies were initially presented the alcoholic preparation and among mothers whose babies were initially presented the oily preparation. Furthermore, the acceptance for the oily preparation was better irrespective of gender of the infant or parity of the mother. In conclusion, from the perspective of mothers, Swiss newborn infants prefer the taste of the oily vitamin D(3) preparation over the alcoholic preparation.

Topics: Body Weight; Choice Behavior; Cholecalciferol; Female; Follow-Up Studies; Gestational Age; Humans; Infant Formula; Infant, Newborn; Male; Mothers; Retrospective Studies; Single-Blind Method; Solutions; Taste; Vitamins

To our knowledge, no rigorously designed clinical trials have evaluated the relation between vitamin D and physician-diagnosed seasonal influenza.. We investigated the effect of vitamin D supplements on the incidence of seasonal influenza A in schoolchildren.. From December 2008 through March 2009, we conducted a randomized, double-blind, placebo-controlled trial comparing vitamin D(3) supplements (1200 IU/d) with placebo in schoolchildren. The primary outcome was the incidence of influenza A, diagnosed with influenza antigen testing with a nasopharyngeal swab specimen.. Influenza A occurred in 18 of 167 (10.8%) children in the vitamin D(3) group compared with 31 of 167 (18.6%) children in the placebo group [relative risk (RR), 0.58; 95% CI: 0.34, 0.99; P = 0.04]. The reduction in influenza A was more prominent in children who had not been taking other vitamin D supplements (RR: 0.36; 95% CI: 0.17, 0.79; P = 0.006) and who started nursery school after age 3 y (RR: 0.36; 95% CI: 0.17, 0.78; P = 0.005). In children with a previous diagnosis of asthma, asthma attacks as a secondary outcome occurred in 2 children receiving vitamin D(3) compared with 12 children receiving placebo (RR: 0.17; 95% CI: 0.04, 0.73; P = 0.006).. This study suggests that vitamin D(3) supplementation during the winter may reduce the incidence of influenza A, especially in specific subgroups of schoolchildren. This trial was registered at https://center.umin.ac.jp as UMIN000001373.

Topics: Adolescent; Body Height; Body Weight; Child; Cholecalciferol; Dietary Supplements; Double-Blind Method; Female; Humans; Influenza A virus; Influenza, Human; Japan; Male; Patient Selection; Placebos; Risk

Some epidemiological and clinical studies have shown that increased dairy consumption or calcium and/or vitamin D supplementation can have a beneficial effect on blood pressure, and lipid and lipoprotein concentrations. The aim of this study was to assess the long-term effects of calcium-vitamin D(3) fortified milk on blood pressure and lipid-lipoprotein concentrations in community-dwelling older men.. This is a substudy of a 2-year randomized controlled trial in which 167 men aged >50 years were assigned to receive either 400 ml per day of reduced fat (approximately 1%) milk fortified with approximately 1000 mg of calcium and 800 IU of vitamin D(3) or to a control group receiving no additional fortified milk. Weight, blood pressure, lipid and lipoprotein concentrations were measured every 6 months. Participants on lipid-lowering (n=32) or antihypertensive medication (n=39) were included, but those who commenced, increased or decreased their medication throughout the intervention were excluded (n=27).. In the 140 men included in this study (milk, n=73; control, n=67), there were no significant effects of the calcium-vitamin D(3) fortified milk on weight, systolic or diastolic blood pressure, total cholesterol, high-density lipoprotein or low-density lipoprotein cholesterol or triglyceride concentrations at any time throughout the intervention. Similar results were observed after excluding men taking antihypertensive or lipid-lowering medication or limiting the analysis to those with baseline calcium intakes <1000 mg per day and/or with hypovitaminosis D (25(OH)D <75 nmol/l).. Supplementation with reduced-fat calcium-vitamin D(3) fortified milk did not have a beneficial (nor detrimental) effect on blood pressure, lipid or lipoprotein concentrations in healthy community-dwelling older men.

Topics: Aged; Animals; Blood Pressure; Body Weight; Calcium; Calcium, Dietary; Cholecalciferol; Food, Fortified; Humans; Lipids; Male; Middle Aged; Milk

Two trials were conducted to determine if thiram-induced tibial dyschondroplasia (TD) in chickens was linked to a vitamin D deficiency and calcium homeostasis dysregulation, and whether feeding vitamin D fortified diets may prevent it. Day-old chickens were given grower diets containing different vitamin D products throughout the experiment until necropsy on day 16. Half of the birds in each feed group received thiram at levels of 100 ppm (trial 1) or 50 ppm (trial 2) between days 7-9 to induce TD. The birds were weighed, bled, and euthanized to determine TD incidences and severity by examining the growth plates. Tibial bones were used to measure biomechanical strength and ash content. Blood concentrations of 25-hydroxyvitamin D, Ca, P, alkaline phosphatase, and creatine kinase were measured in serum that showed no differences between different groups. Thiram reduced body weight and induced TD regardless of any vitamin D treatment to the same extent as untreated birds.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Body Weight; Bone and Bones; Calcitriol; Chickens; Cholecalciferol; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Minerals; Osteochondrodysplasias; Poultry Diseases; Thiram; Vitamin D

A series of experiments was conducted to investigate the effects of maternal dietary vitamin D3 supplementation at 4 different times during the laying cycle, on the performance and bone quality of broiler chicks fed a diet that induced tibial dyschondroplasia (TD) or an adequate diet. Ross x Ross broiler breeder hens were fed a corn-soy diet with various levels of vitamin D3 from 24 to 66 wk of age. Eggs were collected at 39, 44, 53, and 64 wk of age and hatched. Chicks from hens fed 250 IU of D3/kg (low maternal D3 or LMD3) and 2,000 IU of D3/ kg (high maternal D3 or HMD3) levels were placed in battery brooders and fed the diets from 0 to 16 d. At 16 d, the chicks were weighed and killed; the left tibias were used for bone ash determinations, and the right tibias were used to score the incidence and severity of TD (0, 1, 2, or 3, where 3 is the most severe). Body weight gain and feed intake were significantly lower for the LMD3 chicks at wk 44 and 64, although there was no difference in weight at hatch. For the first 2 hatches (wk 39 and 44), the LMD3 and HMD3 chicks demonstrated high average TD scores (2.03 and 1.57 vs. 2.05 and 1.75 for the LMD3 vs. HMD3 chicks, respectively) and high average incidences of severe TD (50 and 35% vs. 45 and 34% for LMD3 vs. HMD3 levels, respectively). However, results from the last 2 hatches (wk 53 and 64) showed that HMD3 chicks, compared with LMD3 chicks, had reduced average TD scores (1.39 and 1.47 vs. 1.01 and 0.44 for LMD3 vs. HMD3 levels, respectively) and severe TD incidence (36 and 40% vs. 17 and 8% for the LMD3 vs. HMD3 levels, respectively). In this experiment, as egg production declined toward the end of the laying cycle, hens fed the HMD3 might have been able to deposit sufficient quantities of vitamin D3 in the egg to maintain excellent body weight gain at 16 d of age and reduce the incidence and severity of TD. Hens fed the LMD3 diet were unable to produce similar improvements.

Topics: Aging; Animal Feed; Animals; Body Weight; Chickens; Cholecalciferol; Dietary Supplements; Dose-Response Relationship, Drug; Feeding Behavior; Female; Osteochondrodysplasias; Rickets; Tibia

An experiment was conducted with 25- to 66-wk-old Ross broiler breeders in an environment excluding ultraviolet light to determine the cholecalciferol (D3) requirements for hen day egg production; hatchability; body weight of the progeny at 1 d; embryo mortality during the early (1 to 10 d of incubation), middle (11 to 15 d of incubation), and late stages (16 to 21 d of incubation) of development; egg weight; specific gravity; and body ash of the progeny at 1 d of age. Five levels of vitamin D3 (125, 250, 500, 1,000, and 2,000 IU/kg of diet) were fed to hens from 25 to 66 wk of age. One additional group was fed no supplemental D3 until 36 wk of age and was then changed to 4,000 IU/kg of diet. Separate regression analyses were performed for wk 27 to 36 (peak original design) and for wk 37 to 66 (postpeak production modified design). The D3 levels for the predicted maximum hen day egg production during peak and postpeak were 1,424 and 2,804 IU/kg, respectively. The D3 levels for the predicted maximum hatchability were 1,390 IU/ kg (peak) and 2,708 IU/kg (postpeak). The level of D3 that resulted in the minimum early embryo mortality was 1,288 IU/kg at peak; however, no significant effect was observed at postpeak. The D3 levels for minimum middle stage embryo mortality were 1,130 IU/kg (peak) and 2,568 IU/kg (postpeak) and for late stage embryo mortality were 1,393 IU/kg (peak) and 2,756 IU/kg (postpeak). The D3 level for maximum egg weight was 1,182 IU/kg (peak) and for specific gravity was 1,337 IU/kg (peak) and >2,000 IU/kg (postpeak). The D3 level for maximum body ash of progeny at d 1 was >2,000 IU/kg. Analysis of the data from the original design of the experiment (treatments providing 0, 125, 250, 500, 1,000, and 2,000 IU of vitamin D3/kg for the 27- to 36-wk-old birds) indicates a requirement of approximately 1,400 IU of D3/kg of feed for broiler breeder hens. When the data from the modified experiment (37 to 66 wk of age) include conversion of the treatment provided at 0 IU of D3/kg to a treatment providing 4,000 IU of D3/kg, the requirement may be approximately 2,800 IU of D3/kg.

Topics: Aging; Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Body Weight; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Feeding Behavior; Female; Reproduction

The long-term effects of calcium and vitamin D supplementation on bone material and structural properties in older men are not known. The aim of this study was to examine the effects of high calcium (1000 mg/day)- and vitamin-D(3) (800 IU/day)-fortified milk on cortical and trabecular volumetric BMD (vBMD) and bone geometry at the axial and appendicular skeleton in men aged over 50 years. One hundred and eleven men who were part of a larger 2-year randomized controlled trial had QCT scans of the mid-femur and lumbar spine (L(1)-L(3)) to assess vBMD, bone geometry and indices of bone strength [polar moment of inertia (I(polar))]. After 2 years, there were no significant differences between the milk supplementation and control group for the change in any mid-femur or L(1)-L(3) bone parameters for all men aged over 50 years. However, the mid-femur skeletal responses to the fortified milk varied according to age, with a split of 62 years being the most significant for discriminating the changes between the two groups. Subsequent analysis revealed that, in the older men (>62 years), the expansion in mid-femur medullary area was 2.8% (P < 0.01) less in the milk supplementation compared to control group, which helped to preserve cortical area in the milk supplementation group (between group difference 1.1%, P < 0.01). Similarly, for mid-femur cortical vBMD and I(polar), the net loss was 2.3 and 2.8% less in the milk supplementation compared to control group (P < 0.01 and <0.001, respectively). In conclusion, calcium-vitamin-D(3)-fortified milk may represent an effective strategy to maintain bone strength by preventing endocortical bone loss and slowing the loss in cortical vBMD in elderly men.

Topics: Aged; Aged, 80 and over; Animals; Body Height; Body Mass Index; Body Weight; Bone and Bones; Bone Density; Calcium; Cholecalciferol; Femur; Food, Fortified; Humans; Male; Middle Aged; Milk; Osteoporosis; Time Factors; Tomography, X-Ray Computed; Treatment Outcome

A 2-year milk intervention trial was carried out with 757 girls, aged 10 years, from nine primary schools in Beijing (April 1999 - March 2001). Schools were randomised into three groups: group 1, 238 girls consumed a carton of 330 ml milk fortified with Ca on school days over the study period; group 2, 260 girls received the same quantity of milk additionally fortified with 5 or 8 microg cholecalciferol; group 3, 259 control girls. Anthropometric and bone mineralisation measurements, as well as dietary, health and physical-activity data, were collected at baseline and after 12 and 24 months of the trial. Over the 2-year period the consumption of this milk, with or without added cholecalciferol, led to significant increases in the changes in height (> or =0.6 %), sitting height (> or =0.8 %), body weight (> or 2.9 %), and (size-adjusted) total-body bone mineral content (> or =1.2 %) and bone mineral density (> or =3.2 %). Those subjects receiving additional cholecalciferol compared with those receiving the milk without added 25-hydoxycholecalciferol had significantly greater increases in the change in (size-adjusted) total-body bone mineral content (2.4 v. 1.2 %) and bone mineral density (5.5 v. 3.2 %). The milk fortified with cholecalciferol significantly improved vitamin D status at the end of the trial compared with the milk alone or control groups. It is concluded that an increase in milk consumption, e.g. by means of school milk programmes, would improve bone growth during adolescence, particularly when Ca intake and vitamin D status are low.

Topics: Analysis of Variance; Animals; Body Height; Body Weight; Bone Density; Bone Development; Calcifediol; Calcium, Dietary; Child; China; Cholecalciferol; Dietary Proteins; Energy Intake; Female; Food, Fortified; Growth; Humans; Milk

The Food and Nutrition Board of the National Academy of Sciences states that 95 microg vitamin D/d is the lowest observed adverse effect level (LOAEL).. Our objective was to assess the efficacy and safety of prolonged vitamin D3 intakes of 25 and 100 microg (1000 and 4000 IU)/d. Efficacy was based on the lowest serum 25-hydroxyvitamin D [25(OH)D] concentration achieved by subjects taking vitamin D3; potential toxicity was monitored by measuring serum calcium concentrations and by calculating urinary calcium-creatinine ratios.. Healthy men and women (n = 61) aged 41 +/- 9 y (mean +/- SD) were randomly assigned to receive either 25 or 100 microg vitamin D3/d for 2-5 mo, starting between January and February. Serum 25(OH)D was measured by radioimmunoassay.. Baseline serum 25(OH)D was 40.7 +/- 15.4 nmol/L (mean +/- SD). From 3 mo on, serum 25(OH)D plateaued at 68.7 +/- 16.9 nmol/L in the 25-microg/d group and at 96.4 +/- 14.6 nmol/L in the 100-microg/d group. Summertime serum 25(OH)D concentrations in 25 comparable subjects not taking vitamin D3 were 46.7 +/- 17.8 nmol/L. The minimum and maximum plateau serum 25(OH)D concentrations in subjects taking 25 and 100 microg vitamin D3/d were 40 and 100 nmol/L and 69 and 125 nmol/L, respectively. Serum calcium and urinary calcium excretion did not change significantly at either dosage during the study.. The 100-microg/d dosage of vitamin D3 effectively increased 25(OH)D to high-normal concentrations in practically all adults and serum 25(OH)D remained within the physiologic range; therefore, we consider 100 microg vitamin D3/d to be a safe intake.

Topics: Adult; Analysis of Variance; Body Weight; Calcifediol; Calcium; Cholecalciferol; Creatinine; Drug Evaluation; Female; Humans; Male; Middle Aged; No-Observed-Adverse-Effect Level; Radioimmunoassay; Safety; Time Factors; Treatment Outcome

Hormone replacement therapy (HRT) prevents postmenopausal bone loss and fractures. However, the occurrence of women with no bone response to HRT has not been widely examined. We identified the densitometric nonresponders to long-term HRT and investigated some characteristics and biochemical variables as possible predictors of densitometric nonresponse in postmenopausal women. The study population was a subsample of the Kuopio Osteoporosis Study (n = 14,220). A total of 464 early postmenopausal women were randomized into four treatment groups: (1) HRT (sequential combination of 2 mg estradiol valerate and 1 mg cyproterone acetate); (2) vitamin D3; (3) HRT + Vitamin D3 combined; and (4) placebo. In this study, the data from HRT and placebo groups were analyzed. Lumbar (L2-4) and femoral neck bone mineral density (BMD) were determined by dual-energy X-ray absorptiometry (DXA) at baseline and after 5 years of treatment. A densitometric nonresponder was defined as a woman whose 5-year BMD change was similar to the mean BMD change (+95% CI) of the placebo group or worse. Altogether, 74 women in the HRT group and 104 women in the placebo group complied with the treatment. According to spinal BMD analysis, 11% of the women were classified as densitometric nonresponders; the corresponding proportion for femoral BMD analysis was 26%. Both smoking (p = 0.003) and low body weight (p = 0.028) were significant risk factors for densitometric nonresponse to HRT. After 6 months of treatment the densitometric nonresponders (hip) had a significantly higher mean serum follicle stimulating hormone (FSH) level (p = 0.038) and lower increases in serum estradiol levels (p = 0.006) than the densitometric responders. The mean changes in serum FSH and alkaline phosphatase levels were significantly lower among the densitometric nonresponders (spine) than responders (p = 0.043 and 0.017, respectively). In conclusion, this prospective study shows that especially current smokers and women with low body weight are at increased risk of poor bone response to HRT. Repeated serum FSH, estradiol and alkaline phosphatase measurements during the first months of long-term HRT may be helpful in identifying the women with no bone response to HRT.

Topics: Alkaline Phosphatase; Biomarkers; Body Weight; Bone and Bones; Bone Density; Cholecalciferol; Estradiol; Estrogen Replacement Therapy; Estrogens; Female; Follicle Stimulating Hormone; Humans; Middle Aged; Osteoporosis, Postmenopausal; Prospective Studies; Smoking; Treatment Failure

We aimed to evaluate whether pulmonary fibrosis occurs in type 2 diabetes rat models and whether VD3 can prevent it by inhibiting pyroptosis.. Sprague-Dawley rats were assigned to normal control (NC), diabetic model control (MC), low-dose VD3 (LVD), medium-dose VD3 (MVD), high-dose VD3 (HVD) and metformin positive control (PC) groups. Type 2 diabetes model was induced by a high-sugar, high-fat diet combined with STZ injection, and subsequently intervened with VD3 or metformin for 10 weeks. Blood glucose, body weight, food intake, water intake, urine volume, morphology, lung hydroxyproline level, immunohistochemistry, TUNEL staining, inflammatory cytokines secretion and related protein expression were analyzed.. Diabetic rats exhibited significant impairments in fasting blood glucose, insulin resistance, body weight, food intake, water intake, and urine volume. While morphological parameters, diabetic rats exhibited severe lung fibrosis. Intriguingly, VD3 intervention reversed, at least in part, the diabetes-induced alterations. The expression of pyroptosis-related proteins was up-regulated in diabetic lungs whereas the changes were reversed by VD3. In the meanwhile, SIRT3 expression was down-regulated in diabetic lungs while VD3 up-regulated it.. Fibrotic changes were observed in diabetic rat lung tissue and our study indicates that VD3 may effectively ameliorate diabetic pulmonary fibrosis via SIRT3-mediated suppression of pyroptosis.

Topics: Animals; Apoptosis; Blood Glucose; Body Weight; Cholecalciferol; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Metformin; Pulmonary Fibrosis; Pyroptosis; Rats; Rats, Sprague-Dawley; Sirtuin 3

Topics: Adolescent; Adult; Body Weight; Cholecalciferol; Humans; Male; Psychomotor Performance; Vitamin D; Vitamins; Young Adult

Limited evidence is available to validate beneficial responses from extra nutrient supplements for mediation of growth suppression that results from immune challenges. Extrarenal roles of vitamin D metabolites in immune function implicate vitamin D3 supplements as a nutrient for potential beneficial effects. The current objective was to assess growth and bone ash responses to dietary vitamin D3 (D) supplements for growing pigs undergoing an immune challenge. At weaning, 216 crossbred pigs (4 pigs/pen, 6 pens/treatment) were randomly allotted within sex and weight blocks to 1 of the 9 treatments. Treatments included D supplements (0, 100, or 800 IU/kg) in a factorial arrangement with 3 vaccine (V) protocols; no injection (0 × V), a single 2 mL injection of a Lawsonia intracellularis vaccine at day 14 (1 × V), or 2 mL injections of the same vaccine at days 0 and 7 (2 × V). An adjustment diet with no supplemental D was fed for 1 wk, then assigned D diets for 2 wk (P2). After P2, all pigs were phase-fed standard diets (D = 280 IU/kg) to assess subsequent growth to 115 kg. No differences due to D supplements or vaccination protocol were detected in ADG (0.233 ± 0.021 kg/d) or GF (0.642 ± 0.028 kg/d) over the 21-d nursery trial; however, ADFI was lower (P < 0.10) in pigs fed D levels of 0 vs. 100 and 800 (0.340 vs. 0.375, 0.372 ± 0.027 kg/d). Bone mineral content (g) from whole-body dual energy X-ray absorptiometry scans at 9 wk (n = 4 pigs/treatment) was lower in pigs fed 0 vs. 100 and 800 IU of D (287 vs. 325, 323 ± 34.1 g/pig). Growth from nursery to 115 kg was lower (P < 0.01) in pigs fed D levels of 0 vs.100 and 800 (0.828 vs. 0.876, 0.889 ± 0.021 kg/d). At market, approximately two-thirds of pigs showed positive L. intracellularis serology titers regardless of treatment. Limited evidence for D-mediation of an immune challenge using the vaccination protocols may be a consequence of limited vaccine effects on growth in the nursery and seroconversion of most pigs to L. intracellularis by market.

Topics: Animal Feed; Animals; Body Weight; Bone Density; Cholecalciferol; Diet; Dietary Supplements; Female; Male; Minerals; Swine; Weaning

Normal vitamin D homeostasis is critical for optimal health; nevertheless, vitamin D deficiency is a worldwide public health problem. Vitamin D insufficiency is most commonly due to inadequate cutaneous synthesis of cholecalciferol and/or insufficient intake of vitamin D, but can also arise as a consequence of pathological states such as obesity. Serum concentrations of 25(OH)D (calcidiol) are low in obesity, and fail to increase appropriately after vitamin D supplementation. Although sequestration of vitamin D in adipose tissues or dilution of ingested or cutaneously synthesized vitamin D in the large fat mass of obese patients has been proposed to explain these findings, here we investigate the alternative mechanism that reduced capacity to convert parent vitamin D to 25(OH)D due to decreased expression of CYP2R1, the principal hepatic vitamin D 25-hydroxylase. To test this hypothesis, we isolated livers from female mice of 6 to 24 weeks of age, weaned onto either a normal chow diet or a high-fat diet, and determined the abundance of Cyp2r1 mRNA using digital droplet-quantitative PCR. We observed a significant (p < 0.001) decrease in Cyp2r1 mRNA in the liver of high-fat diet-fed mice relative to lean-chow-fed female mice. Moreover, there was a significant (p < 0.01) relationship between levels of Cyp2r1 mRNA and serum 25(OH)D concentrations as well as between Cyp2R1 mRNA and the ratio of circulating 25(OH)D3 to cholecalciferol (p < 0.0001). Using linear regression we determined a curve with 25(OH)D3/cholecalciferol versus normalized Cyp2R1 mRNA abundance with an R

Topics: Animals; Body Weight; Calcifediol; Cholecalciferol; Cholestanetriol 26-Monooxygenase; Diet, High-Fat; Female; Liver; Mice, Inbred C57BL; Mice, Obese; Obesity; RNA, Messenger; Thinness; Vitamin D

The effect of vitamin D on cardiac dysfunction after menopause is still under investigation. Therefore, we investigated the effect of vitamin D3 on cardiac apoptotic and structural changes in ovariectomized rats. Forty adult female albino rats were divided into 4 equal groups: sham rats, sham rats treated with vitamin D3, ovariectomized rats, and ovariectomized rats treated with vitamin D3 (500 IU/kg per day for 6 weeks, orally). Body mass, blood pressure, heart rate, and whole heart mass (WHM) were measured. Serum soluble receptors of advanced glycation end products (sRAGE), C-reactive protein, malondialdehyde, and total antioxidant capacity were estimated. Cardiac sections were stained with haematoxylin-eosin and Masson's trichrome stain. Fas and FasL apoptosis-related proteins were detected by immunohistochemistry. Vitamin D3 treatment significantly decreased ovariectomy-induced cardiac Fas and FasL apoptosis-related proteins, whole heart mass, body mass, C-reactive protein, and malondialdehyde accompanied by decreased inflammation and reduced collagen deposition between cardiac muscle fibres. However, vitamin D3 significantly increased total antioxidant capacity and sRAGE in ovariectomized and sham treated groups. Our findings suggest that vitamin D3 treatment can prevent ovariectomy-induced cardiac structural and apoptotic changes in rats via increasing sRAGE and antioxidant activity. Our results suggest that vitamin D3 has therapeutic effect against postmenopausal cardiovascular disease.

Topics: Animals; Apoptosis; Biomarkers; Body Weight; Cholecalciferol; Dietary Supplements; Estrogens; Fas Ligand Protein; fas Receptor; Female; Myocardium; Ovariectomy; Oxidative Stress; Rats; Rats, Sprague-Dawley; Receptor for Advanced Glycation End Products

The prevalence of vitamin D deficiency in nursing home residents ranges from 79% to 98%.. The aim of this cross-sectional observational study in somatic and psychogeriatric nursing home residents was to determine the efficacy of a standardized oral vitamin D dosing regimen (VDDR) consisting of a loading dose (LD) of cholecalciferol 200,000 IU followed by a maintenance dose (MD) of 100,000 IU every 13 weeks in obtaining and maintaining an adequate and safe vitamin D trough level (VDTL), defined as 75-220 nmol/L (reference range).. Blood samples of nursing home residents who had received the LD followed by at least one MD were analyzed for VDTL, calcium, parathyroid hormone, and creatinine. Data on age, sex, race, body weight and height, co-morbidity, co-medication, number of MDs, calcium supplementation, smoking, and use of alcohol were obtained from patient charts. The primary outcome for the efficacy of the VDDR was the percentage of nursing home residents with a VDTL 75-220 nmol/L, with a target percentage of 85% for the dosing regimen to be considered efficacious.. In 91 (58%; 95% confidence interval [CI] 50-66) of 156 included nursing home residents, a VDTL within the reference range was measured (mean [standard deviation] 81 [28] nmol/L, range 13-150 nmol/L). The only variable that was identified as a significant risk indicator for obtaining a VDTL ≥ 75 nmol/L was the number of MDs being four or more (≥ 4 vs. < 4; odds ratio 2.7; 95% CI 1.4-5.3).. This standardized VDDR was not efficacious in obtaining and maintaining an adequate VDTL in this nursing home resident population.. NTR6029 (The Netherlands National Trial Register).

Topics: Aged; Aged, 80 and over; Body Weight; Calcium; Cholecalciferol; Creatinine; Cross-Sectional Studies; Dose-Response Relationship, Drug; Female; Humans; Male; Middle Aged; Netherlands; Nursing Homes; Parathyroid Hormone; Prevalence; Vitamin D Deficiency; Vitamins

The aim of this study was to determine whether calcium potentiates acute carbon tetrachloride (CCl4) -induced toxicity. Elevated calcium levels were induced in mice by pre-treatment with cholecalciferol (vitamin D3; V.D3), a compound that has previously been shown to induce hypercalcemia in human and animal models. As seen previously, mice injected with CCl4 exhibited increased plasma levels of alanine aminotransferase, aspartate aminotransferase, and creatinine; transient body weight loss; and increased lipid peroxidation along with decreased total antioxidant power, glutathione, ATP, and NADPH. Pre-treatment of these animals with V.D3 caused further elevation of the values of these liver functional markers without altering kidney functional markers; continued weight loss; a lower lethal threshold dose of CCl4; and enhanced effects on lipid peroxidation and total antioxidant power. In contrast, exposure to V.D3 alone had no effect on plasma markers of liver or kidney damage or on total antioxidant power or lipid peroxidation. The potentiating effect of V.D3 was positively correlated with elevation of hepatic calcium levels. Furthermore, direct injection of CaCl2 also enhanced CCl4-induced hepatic injury. Since CaCl2 induced hypercalcemia transiently (within 3 h of injection), our results suggest that calcium enhances the CCl4-induced hepatotoxicity at an early stage via potentiation of oxidative stress.

Topics: Adenosine Triphosphate; Animals; Body Weight; Calcium; Carbon Tetrachloride; Cholecalciferol; Cytochrome P-450 CYP2E1; Hypercalcemia; Lipid Peroxidation; Liver; Male; Malondialdehyde; Mice; NADP; Oxidative Stress

Vitamin D (25(OH)D3) is an essential nutrient that plays a role in the immune system. Serum 25(OH)D3 is found to be associated with asthma. However, the role of vitamin D in obese asthma remains unclear. Therefore, we investigated the association between vitamin D levels and asthma outcomes in a murine model of obese asthma. We also evaluated NLRP3 inflammasome activity in the pathogenesis of obese asthma. We divided 20 male Balb/c mice (3-4 weeks old) into 4 groups: normal control, asthma, obese, and obese asthma and developed an obese asthma mouse model. Airway hyperreactivity, cytokine concentrations, 25(OH)D3 levels, NLRP3 mRNA and IL-1β mRNA expressions were measured. Lung histology and bronchoalveolar lavage fluid (BALF) cell count were also determined. Obese asthma mice showed a significant increase in airway hyper-responsiveness, airway inflammation, pro-inflammatory cytokine levels and NLRP3 mRNA, IL-1β mRNA expression. Both asthma and obese groups had lower 25(OH)D3 levels. Vitamin D levels in obese asthma were the lowest among all groups. Vitamin D levels correlated negatively with body weight, lung resistance levels at 25 mg/mL of methacholine, total inflammatory cells, and IL-1β and IL-17 concentrations in BALF. These data demonstrated an association between serum vitamin D levels and outcomes of obese asthma, and indicated that NLRP3 inflammasome may play a role in this disorder.

Topics: Animals; Asthma; Body Weight; Bronchoalveolar Lavage Fluid; Cholecalciferol; Cytokines; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Leukocyte Count; Lung; Male; Mice, Inbred BALB C; NLR Family, Pyrin Domain-Containing 3 Protein; Obesity; Real-Time Polymerase Chain Reaction; Time Factors

Recent evidence suggests that 1α,25-dihydroxyvitamin D3 (calcitriol, VD3), the active form of vitamin D (VD), can inhibit the proliferation of microorganisms. In the present study, we conducted in vitro experiments and utilized in vivo murine models to investigate the antimalarial activity of VD3 and its analog, 22-oxacalcitriol (22-OCT), which was designed to cause less hypercalcemia than VD3. VD3 and 22-OCT treatments effectively resolved a Plasmodium chabaudi (Pc) infection in wild-type mice. Reduced parasitemia was observed during the acute phase of infection in the presence of VD3 and 22-OCT, followed by a delayed peak during the chronic stage of infection. Some anti-Pc activity was observed in VD receptor knockout (KO) mice. VD3 and 22-OCT also completely inhibited the proliferation of P. falciparum (Pf) in human red blood cells in vitro. Plasma levels of interferon (IFN)-γ in VD3-treated B10 and B6 mice were lower than those in vehicle-treated animals, and VD3 resolved a Pc infection in IFN-γ-KO mice, which greatly improved survival. These data suggest that the protective effects of VD3 are elicited through an IFN-γ-independent mechanism. Effective antiplasmodial doses of VD3 and 22-OCT resulted in a loss of body weight in mice. This loss in body weight occurred concomitantly with the development of hypercalcemia. Zoledronic acid partially attenuated VD3-induced hypercalcemia and abrogated the antiparasitic effects of VD3. This study highlights a potential therapeutic role for VD3 in the treatment of malarial infections and shows that hypercalcemia is excellent indicator of the antiplasmodial activity of VD3.

Topics: Acute Disease; Animals; Antimalarials; Body Weight; Calcitriol; Cholecalciferol; Chronic Disease; Diphosphonates; Erythrocytes; Humans; Hypercalcemia; Imidazoles; Interferon-gamma; Malaria; Mice; Mice, Inbred BALB C; Mice, Knockout; Parasitemia; Plasmodium chabaudi; Receptors, Calcitriol; Zoledronic Acid

The aim of this study was to determine the bone mineral density (BMD) and the factors leading to reduction in BMD in children diagnosed with meningomyelocele.. A total of 31 patients with meningomyelocele (mean (SD) age, 8.5 (3.9) years; 51.6%were females) and 22 healthy children were included. BMD of femoral neck and spinal L1– L4 levels and markers for bone metabolism were recorded.. BMD of femoral neck (p=0.001) and spinal L1–L4 (p = 0.01), serum calcium (p = 0.031), and urinary deoxypyridinoline (p=0.015) levels were significantly lower in patients than in controls. Mobilization was significantly reduced in lumbar (p=0.001) and thoracic (p=0.002) level meningomyelocele compared to controls, while a significant positive correlation was noted between BMD of spinal L1–L4 and mobility (r=0.58, p=0.015).. Our findings suggest a decrease in BMD in meningomyelocele patients being associated with osteoporosis rather than nutritional and hormonal factors and the negative impact of higher levels of lesion on the mobility.

Topics: Absorptiometry, Photon; Adolescent; Adrenocorticotropic Hormone; Amino Acids; Anthropometry; Blood Chemical Analysis; Body Weight; Bone Density; Calcium; Case-Control Studies; Chi-Square Distribution; Child; Child, Preschool; Cholecalciferol; Female; Follicle Stimulating Hormone; Humans; Male; Meningomyelocele; Statistics as Topic

Multiple sclerosis (MS) is an immune-mediated demyelinating disorder of the central nervous system (CNS). We described that Candida albicans (Ca) aggravates experimental autoimmune encephalomyelitis (EAE) that is a model to study MS. We also observed that vaccination with a myelin peptide (MOG) in the presence of vitamin D (VitD) protected mice against EAE. In this work, we investigated whether Ca infection interferes with the efficacy of this vaccine.. EAE was induced in C57BL/6 female mice previously vaccinated with MOG+VitD and then infected 3 days before encephalomyelitis induction.. Vaccination was able to control EAE development in infected mice. These animals gained weight, and only a few progressed to very low clinical scores. Protection was confirmed by a lower inflammatory infiltration in the CNS and was also associated with a reduced production of encephalitogenic cytokines by spleen and CNS cell cultures. The elevated percentage of CD25(+) FoxP3(+) cells suggests that regulatory T cells are involved in the protection. Adoptive transfer of splenocytes from mice vaccinated with MOG+VitD supports the view that protection is mediated by immunoregulatory cells.. Together, these experiments provide evidence demonstrating that EAE can be prevented by the inverse vaccination with MOG+VitD even in the presence of a disease-aggravating infectious agent.

Topics: Animals; Body Weight; Candida albicans; Candidiasis; Cells, Cultured; Central Nervous System; Cholecalciferol; Cytokines; Dendritic Cells; Disease Models, Animal; Down-Regulation; Encephalomyelitis, Autoimmune, Experimental; Female; Forkhead Transcription Factors; Indoleamine-Pyrrole 2,3,-Dioxygenase; Lymph Nodes; Mice; Mice, Inbred C57BL; Myelin-Oligodendrocyte Glycoprotein; Vitamins

Deficiencies in vitamin D directly impact children's health and place minority and obese youth at risk for a range of health issues. The Institute of Medicine (IOM) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium has set both a recommended daily allowance (RDA) for vitamin D supplementation and a population-wide sufficiency target for the biomarker of vitamin D status, serum 25-hydroxyvitamin D (25(OH)D). However, new research suggests that the RDA is not sufficient to meet the target biomarker status for individuals who are heavy or who have dark skin. Our objective was to provide appropriate daily vitamin D supplementation levels for these individuals.. Using data derived from the National Health and Nutrition Examination Survey (NHANES) and a recently published dosing formula, we calculated the required supplemental dose of vitamin D to meet the IOM target in children and adolescents.. To be sure that 95% of the target population meets the IOM's population-wide biomarker target, some individuals require a daily dose of up to 2,000 international units (IUs) of supplemental vitamin D.. Health professionals should work with their patients to encourage lifelong vitamin D supplement use at a dosage sufficient to obtain adequate 25(OH)D levels.

Topics: Adolescent; Body Weight; Calcifediol; Child; Cholecalciferol; Dietary Supplements; Dose-Response Relationship, Drug; Drug Dosage Calculations; Humans; Recommended Dietary Allowances; Skin Pigmentation

Meningoencephalitis caused by Escherichia coli is associated with high rates of mortality and risk of neurological sequelae in newborns and infants and in older or immunocompromised adults. A high prevalence of neurological disorders has been observed in geriatric populations at risk of hypovitaminosis D.. In vivo, we studied the effects of vitamin D3 on survival and the host's immune response in experimental bacterial meningoencephalitis in mice after intracerebral E. coli infection. To produce different systemic vitamin D3 concentrations, mice received a low, standard, or high dietary vitamin D3 supplementation. Bacterial titers in blood, spleen, and brain homogenates were determined. Leukocyte infiltration was assessed by histological scores, and tissue cytokine or chemokine concentrations were measured.. Mice fed a diet with low vitamin D3 concentration died earlier than control animals after intracerebral infection. Vitamin D deficiency did not inhibit leukocyte recruitment into the subarachnoid space and did not lead to an increased density of bacteria in blood, spleen, or brain homogenates. The release of proinflammatory interleukin (IL)-6 was decreased and the release of anti-inflammatory IL-10 was increased in mice fed a diet with high vitamin D3 supplementation.. Our observations suggest a detrimental role of vitamin D deficiency in bacterial central nervous system infections. Vitamin D may exert immune regulatory functions.

Topics: Analysis of Variance; Animals; Bacterial Load; Body Weight; Central Nervous System; Cholecalciferol; Cytokines; Dietary Supplements; Disease Models, Animal; Escherichia coli; Escherichia coli Infections; Gene Expression Regulation; Meningoencephalitis; Mice; Mice, Inbred C57BL; Spleen; Time Factors; Vitamin D Deficiency

A growing body of evidence suggests that immune activation and inflammatory mediators may play a key role in the development and progression of left ventricle (LV) hypertrophy. The present study was designed to test the hypothesis that the cardioprotective effect of cholecalciferol (Vit-D3) is mediated via the regulation of messenger RNA (mRNA) expression of pro-inflammatory cytokines. Rats were randomly divided into four groups: control group received normal saline (0.9 % NaCl) i.p. for 14 days; Vit-D3 group received Vit-D3 at a dose of 12 μg/kg/day by gavage for 14 days; ISO group received saline for 7 days, and at day 7, ISO (5 mg/kg/day) was injected i.p. for 7 consecutive days to induce cardiac hypertrophy; and Vit-D3 + ISO group was treated with Vit-D3 for 14 days, and at day 7, ISO was administered for 7 consecutive days. Heart/body weight ratio, troponin-T, creatine kinase-MB, and tumor necrosis factor-α (TNF-α) levels of LV tissue were estimated. Levels of mRNA expression of NF-кB (NF-кB)/p65 and inhibitory kappa B (IкB)-α were determined by real-time PCR. Vit-D3 administration before and during induction of cardiac hypertrophy significantly reduced (P < 0.001) cardiac biomarkers. The histopathological examination further confirmed these results. In addition, Vit-D3 significantly decreased (P < 0.001) NF-кB-p65 mRNA expression and increased (P < 0.01) IкB-α mRNA expression in LV tissues compared to ISO group. Based on these findings, it was concluded that the administration of cholecalciferol markedly attenuated the development of ISO-induced cardiac hypertrophy likely through downregulation of TNF-α /NF-кb/p65 signaling pathways. However, it should be pointed out that other signaling pathways may contribute to the cardioprotective effect of Vit-D3 which requires further investigation.

Topics: Animals; Body Weight; Cardiotonic Agents; Cholecalciferol; Hypertrophy, Left Ventricular; I-kappa B Proteins; Isoproterenol; Male; Myocytes, Cardiac; NF-kappa B; Organ Size; Rats, Wistar; Signal Transduction; Transcription Factor RelA; Troponin T; Tumor Necrosis Factor-alpha

Vitamin D deficiency is highly prevalent in dialysis patients. Whether substitution of native vitamin D in these patients is beneficial is a matter of ongoing discussion, as is the optimal dosing schedule. The purpose of this study was to investigate the efficacy and safety of a body-weight adapted oral dosing regimen of cholecalciferol in dialysis patients.. In a prospective single-center study 56 prevalent dialysis patients with a baseline 25OHD3 level <20 ng/mL received 100 IU of cholecalciferol per kg body weight once weekly orally for 26 weeks. 25OHD3 was measured at baseline and at study end, iPTH every three months, serum calcium and phosphorous monthly. Concurrent medication including phosphate binders, calcitriol and cinacalcet and dialysate calcium concentration remained unchanged throughout the study.. Baseline 25OHD3 was 9.9 ± 4.1 ng/mL and increased to 26.1 ± 8.8 ng/mL (P = 0.01). Fourteen patients (27 %) achieved a level > 30 ng/mL and all others above 20 ng/mL. Cinacalcet therapy was positively associated with the increase in 25OHD3 (P = 0.024). The plasma iPTH level significantly decreased from median 362 pg/mL to 297 pg/mL (P = 0.01). This decline was more pronounced in patients with higher baseline iPTH levels (P < 0.01) and differed significantly dependent on concurrent calcitriol therapy. A significant iPTH decrease was observed in patients receiving calcitriol (P = 0.031). Serum calcium and phosphorous did not change significantly throughout the study period. Cholecalciferol substitution was well tolerated without adverse effects.. The dosing regimen of oral cholecalciferol supplementation with 100 IU per kg body weight per week for 26 weeks in dialysis patients with vitamin D deficiency causes a significant increase in 25OHD3 close to the supposed target level of 30 ng/mL and a significant reduction in iPTH, without affecting serum calcium or phosphorous levels.

Topics: Administration, Oral; Aged; Aged, 80 and over; Body Weight; Calcifediol; Calcimimetic Agents; Calcitriol; Calcium; Cholecalciferol; Cinacalcet; Drug Dosage Calculations; Drug Substitution; Female; Humans; Male; Middle Aged; Parathyroid Hormone; Phosphorus; Prospective Studies; Renal Dialysis; Renal Insufficiency, Chronic; Vitamin D Deficiency; Vitamins

Diabetes is associated with long-term complications in the brain and reduced cognitive ability. Vitamin D3 (VD3 ) appears to be involved in the amelioration of hyperglycaemia in streptozotocin (STZ)-induced diabetic rats. Our aim was to analyse the potential of VD3 in avoiding brain damage through evaluation of acetylcholinesterase (AChE), Na(+) K(+) -adenosine triphosphatase (ATPase) and delta aminolevulinate dehydratase (δ-ALA-D) activities and thiobarbituric acid reactive substance (TBARS) levels from cerebral cortex, as well as memory in STZ-induced diabetic rats. Animals were divided into eight groups (n = 5): control/saline, control/metformin (Metf), control/VD3 , control/Metf + VD3 , diabetic/saline, diabetic/Metf, diabetic/VD3 and diabetic/Metf + VD3 . Thirty days after treatment, animals were submitted to contextual fear-conditioning and open-field behavioural tests, after which they were sacrificed and the cerebral cortex was dissected. Our results demonstrate a significant memory deficit, an increase in AChE activity and TBARS levels and a decrease in δ-ALA-D and Na(+) K(+) -ATPase activities in diabetic rats when compared with the controls. Treatment of diabetic rats with Metf and VD3 prevented the increase in AChE activity when compared with the diabetic/saline group. In treated diabetic rats, the decrease in Na(+) K(+) -ATPase was reverted when compared with non-treated rats, but the increase in δ-ALA-D activity was not. VD3 prevented diabetes-induced TBARS level and improved memory. Our results show that VD3 can avoid cognitive deficit through prevention of changes in important enzymes such as Na(+) K(+) -ATPase and AChE in cerebral cortex in type 1 diabetic rats.

Topics: Acetylcholinesterase; Animals; Blood Glucose; Body Weight; Cerebral Cortex; Cholecalciferol; Diabetes Mellitus, Type 1; Eating; Fear; Hypoglycemic Agents; Male; Memory; Metformin; Porphobilinogen Synthase; Rats, Wistar; Sodium-Potassium-Exchanging ATPase; Streptozocin; Thiobarbituric Acid Reactive Substances; Vitamins

Recent findings show that developmental vitamin D deficiency leads to altered brain morphology and behavioral development in the rat offspring. We examined the effects of different dietary vitamin D levels in rat dams on behavior and biochemistry of the offspring. Females were divided into five conditions and received diets containing 0, 1,5, 3.3, 6.0, or 10.0 IU/g of vitamin D₃ from mating to weaning. Offspring were tested as juveniles and as adults for anxiety, social learning and behavior, and locomotion. Results show that both deficient and excessive levels of vitamin D3 in juveniles lead to altered physiology and behavior. In juveniles but not adults, variations in vitamin D were related to variations in measures of anxiety and marginally, activity levels. For social behaviors, both juveniles and adults were affected by mothers' diets. In general, offspring of animals receiving abnormal concentrations of vitamin D showed the most deficits.

Topics: Animals; Behavior, Animal; Body Weight; Cholecalciferol; Female; Lactation; Learning; Male; Motor Activity; Pregnancy; Prenatal Exposure Delayed Effects; Rats; Rats, Sprague-Dawley; Social Behavior

We previously demonstrated that dietary vitamin D(3) at 10x the adequate intake (AI) attenuates the decline in functional capacity in the G93A mouse model of ALS. We hypothesized that higher doses would elicit more robust changes in functional and disease outcomes.. To determine the effects of dietary vitamin D(3) at 50xAI on functional outcomes (motor performance, paw grip endurance) and disease severity (clinical score), as well as disease onset, disease progression and lifespan in the transgenic G93A mouse model of ALS.. Starting at age 25 d, 100 G93A mice (55 M, 45 F) were provided ad libitum with either an adequate (AI; 1 IU D(3)/g feed) or high (HiD; 50 IU D(3)/g feed) vitamin D(3) diet.. HiD females consumed 9% less food corrected for body weight vs. AI females (P = 0.010). HiD mice had a 12% greater paw grip endurance over time between age 60-141 d (P = 0.015), and a 37% greater score during disease progression (P = 0.042) vs. AI mice. Although HiD females had a non-significant 31% greater CS prior to disease onset vs. AI females, they exhibited a significant 20% greater paw grip endurance AUC (P = 0.020) when corrected for clinical score.. Dietary D(3) supplementation at 50x the adequate intake attenuated the decline in paw grip endurance, but did not influence age at disease onset, hindlimb paralysis or endpoint in the transgenic G93A mouse model of ALS. Furthermore, females may have reached the threshold for vitamin D(3) toxicity as evidence by reduced food intake and greater disease severity prior to disease onset.

Topics: Amyotrophic Lateral Sclerosis; Animals; Body Weight; Cholecalciferol; Dietary Supplements; Disease Models, Animal; Disease Progression; Eating; Female; Hand Strength; Hindlimb; Male; Mice; Mice, Transgenic; Physical Endurance; Psychomotor Performance

The introduced Australian brushtail possum is a major vertebrate pest in New Zealand, with impacts on conservation and agriculture being managed largely through poisoning operations. Cholecalciferol (vitamin D3) is registered for use in controlling possums and despite its many advantages it is expensive and relatively inhumane. Combination of a high proportion of aspirin with a low proportion of cholecalciferol was effective in killing high proportions of groups of acclimatised, caged possums: this is attributed to both an unexpectedly high toxicity of the type of cholecalciferol used, and a proposed synergistic mechanism between the two compounds. Death was caused by localised damage to heart ventricles by aspirin, and inhibition of tissue repair by both aspirin and cholecalciferol. The observed toxicosis had lower impact on the welfare of possums than either compound administered alone, particularly aspirin alone. Residue analyses of bait remains in the GI tract suggested a low risk of secondary poisoning by either compound. The combination of cholecalciferol and aspirin has the potential to meet key requirements of cost-effectiveness and humaneness in controlling possum populations, but the effect of the combination in non-target species has yet to be tested.

Topics: Animals; Aspirin; Body Weight; Cholecalciferol; Drug Synergism; Female; Gastrointestinal Tract; Introduced Species; Lethal Dose 50; Male; New Zealand; Pest Control; Trichosurus

This study investigated the effect of insulin and vitamin D(3) (VD(3)) treatment on implant osseointegration in diabetic mellitus (DM) rats. DM was induced by administration of streptozotocin in rats, which received implants insertion in the femur. Then animals were subjected to different treatment and divided to the following group: control, diabetic, insulin-treated diabetic, VD(3)-treated diabetic, insulin and VD(3) combination-treated diabetic rats. The glucose levels and weight of rats were periodically evaluated, and serum 25(OH)D(3) levels in rats were measured at the end of the experiment. Animals were sacrificed at 12 weeks after surgery, the peri-implant trabecular microstructure, implant fixation and implant osseointegration were measured by microscopic computerized tomography (micro-CT) evaluation, push-out test and histomorphometric analysis. Diabetic rats displayed significantly higher blood glucose level, lower body weight, lower serum 25(OH)D(3) levels, and less implant osseointegration than controls. Insulin treatment showed restorative effect on body weight and serum 25(OH)D(3) levels of diabetic rats, but the blood glucose level in diabetic rats were still substantially higher compared to controls after 14 days therapy of insulin. Combined treatment restored hyperglycemia in diabetic rats to be normal, and reversed the impaired osseointegration capacity of implants, with the bone volume ratio and percent osseointegration increased by 1.37-fold and 1.6-fold in micro-CT evaluation, the maximal push-out force and ultimate shear strength by 1.3-fold and 2.1-fold in push-out test, and the bone-to-implant contact and bone area ratio increased by 2.57-fold and 1.44-fold in histomorphometric analysis. Monotreatment also enhanced implant fixation, but less. These results indicated that insulin and VD(3) combined treatment may be an effective approach to enhance implant fixation in diabetic rats, but whether the results could be extrapolated to human needs further study.

Topics: Animals; Blood Glucose; Body Weight; Cholecalciferol; Diabetes Mellitus, Experimental; Insulin; Male; Osseointegration; Prostheses and Implants; Rats; Rats, Wistar; Titanium; Tomography, X-Ray Computed

As decreased bone mineral density (BMD) is a common problem in cystic fibrosis (CF) and milk products may have pivotal dietary role affecting BMD, we aimed to assess the potential influence of adult-type hypolactasia (ATH) and lactose malabsorption (LM) on BMD in adolescent and young adult patients. In 95 CF pancreatic-insufficient patients aged 10-25 years (without liver cirrhosis, steatosis and cholestasis, diabetes mellitus, systemic glucocorticoid therapy), lumbar BMD, the nutritional status, pulmonary function, vitamin D3 concentration, calcium intake and single-nucleotide polymorphism upstream of the lactase gene were assessed. In subjects with the -13910 C/C genotype predisposing to ATH, the presence of LM was determined with the use of a hydrogen-methane breath test (BT). BMD and calcium intake were significantly lower in patients with the C/C genotype (P<0.028 and P<0.043, respectively). The abnormal BMD was stated more frequently in patients with the C/C genotype (P<0.042) and with LM (P<0.007). BMD, daily calcium intake and serum vitamin D concentration were significantly lower in LM subjects than in the other patients (P<0.037, P<0.000004 and P<0.0038, respectively). In logistic regression analysis, the relationship between examined parameters and BMD, was found to be statistically significant (P<0.001). However, only standardized body weight and LM were documented to influence BMD (P<0.025 and P<0.044, respectively). In conclusion, LM seems to be an independent risk factor for decreased BMD in CF patients.

Topics: Adult; Body Weight; Bone Demineralization, Pathologic; Bone Density; Breath Tests; Calcium; Child; Cholecalciferol; Cystic Fibrosis; Female; Humans; Lactase; Lactose Intolerance; Male; Polymorphism, Single Nucleotide; Promoter Regions, Genetic; Risk Factors

1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3) or calcitriol], the hormonally active vitamin D metabolite, exhibits anticancer actions in models of breast cancer and prostate cancer. Because CYP27B1 (1α-hydroxylase), the enzyme catalyzing 1,25(OH)(2)D(3) formation in the kidney, is also expressed in extrarenal tissues, we hypothesize that dietary vitamin D(3) will be converted to 25(OH)D(3) in the body and then to 1,25(OH)(2)D(3) locally in the cancer microenvironment in which it will exert autocrine/paracrine anticancer actions. Immunocompromised mice bearing MCF-7 breast cancer xenografts showed significant tumor shrinkage (>50%) after ingestion of a vitamin D(3)-supplemented diet (5000 IU/kg) compared with a control diet (1000 IU/kg). Dietary vitamin D(3) inhibition of tumor growth was equivalent to administered calcitriol (0.025, 0.05, or 0.1 μg/mouse, three times a week). Both treatments equivalently inhibited PC-3 prostate cancer xenograft growth but to a lesser extent than the MCF-7 tumors. Calcitriol at 0.05 μg and 0.1 μg caused modest but statistically significant increases in serum calcium levels indicating that the dietary vitamin D(3) comparison was to a maximally safe calcitriol dose. Dietary vitamin D(3) did not increase serum calcium, demonstrating its safety at the concentration tested. The vitamin D(3) diet raised circulating 1,25 dihydroxyvitamin D levels and did not alter CYP27B1 mRNA in the kidney but increased it in the tumors, suggesting that extrarenal sources including the tumors contributed to the elevated circulating 1,25 dihydroxyvitamin D(3). Both calcitriol and dietary vitamin D(3) were equipotent in suppressing estrogen synthesis and signaling and other proinflammatory and growth signaling pathways. These preclinical data demonstrate the potential utility of dietary vitamin D(3) supplementation in cancer prevention and therapy.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Body Weight; Breast Neoplasms; Calcitriol; Calcium; Cell Line, Tumor; Cholecalciferol; Dietary Supplements; Estrogen Receptor alpha; Female; Gene Expression Regulation, Neoplastic; Humans; Immunohistochemistry; Male; Mice; Mice, Nude; Ovariectomy; Prostatic Neoplasms; Receptors, Calcitriol; Reverse Transcriptase Polymerase Chain Reaction; Steroid Hydroxylases; Tumor Burden; Vitamin D3 24-Hydroxylase; Vitamins; Xenograft Model Antitumor Assays

Chronic alcohol abuse results in decreased bone mineral density (BMD), which can lead to increased fracture risk. In contrast, low levels of alcohol have been associated with increased BMD in epidemiological studies. Alcohol's toxic skeletal effects have been suggested to involve impaired vitamin D/calcium homeostasis. Therefore, dietary vitamin D supplementation may be beneficial in reducing bone loss associated with chronic alcohol consumption. Six-week-old female C57BL/6J mice were pair-fed ethanol (EtOH)-containing liquid diets (10 or 36% total calories) for 78 days. EtOH exposure at 10% calories had no effects on any measured bone or serum parameter. EtOH consumption at 36% of calories reduced BMD and bone strength (P<0.05), decreased osteoblastogenesis, increased osteoclastogenesis, suppressed 1,25-hydroxyvitamin D3 [1,25(OH)2D3] serum concentrations (P<0.05), and increased apoptosis in bone cells compared with pair-fed controls. In a second study, female mice were pair-fed 30% EtOH diets with or without dietary supplementation with vitamin D3 (cholecalciferol; VitD) for 40 days. VitD supplementation in the EtOH diet protected against cortical bone loss, normalized alcohol-induced hypocalcaemia, and suppressed EtOH-induced expression of receptor of nuclear factor-κB ligand mRNA in bone. In vitro, pretreatment of 1,25(OH)2D3 in osteoblastic cells inhibited EtOH-induced apoptosis. In EtOH/VitD mice circulating 1,25(OH)2D3 was lower compared with mice receiving EtOH alone (P<0.05), suggesting increased sensitivity to feedback control of VitD metabolism in the kidney. These findings suggest dietary VitD supplementation may prevent skeletal toxicity in chronic drinkers by normalizing calcium homeostasis, preventing apoptosis, and suppressing EtOH-induced increases in bone resorption.

Topics: Animals; Apoptosis; Biomechanical Phenomena; Body Composition; Body Weight; Bone Density; Bone Marrow; Bone Remodeling; Cells, Cultured; Central Nervous System Depressants; Cholecalciferol; Ethanol; Female; Femur; Gene Expression; Humans; Mice; Mice, Inbred C57BL; Osteoblasts; Osteoclasts; Osteoporosis, Postmenopausal; RNA; Tomography, X-Ray Computed; Vitamin D; Vitamins; Weight Gain

The study was undertaken to find out the effects of over supplementation of dietary calcium and vitamin D3 on the mineralization of growing skeleton, taking rabbit as an animal model; further to study the effects of Nandrolone deconoate and TGF-beta1 on the mineralization of osteopenic bones. Twenty four New Zealand White rabbits of either sex, 60 day old, were randomly divided in 4 equal groups, A, B, C and D. The animals of groups B, C and D were administered with oral supplementation of calcium (2000 mg/kg of standard rabbit feed) and vit-D3 (1000 IU/kg of standard feed) for 60 days. The animals of group A were given standard ration without any supplementation. After 60 days, the Ca-vit.D3 supplementation was discontinued; and the animals of group C were administered with TGF-beta1 (10 ng, i.m.) once in every three days and animals of group D were given Nandrolone deconoate (10 mg, i.m.) once every week for 30 days, whereas in animals of group B, no treatment was given. All the animals were evaluated based on different observations like body weight, radiographic observations, circulating biochemical and hormone profile (plasma Ca, IP, AP, OC and iPTH) every 15 days up to 60 days after initiation of treatment. The results indicated that the body weight of rabbits in different groups increased gradually and steadily at different intervals till the end of observation period, however, the increase was non-significantly more in group D. The CI in group A increased gradually at different intervals; whereas in groups B, C and D, there was no appreciable increase in the CI during the period of Ca-vit.D3 supplementation, suggesting development of osteopenia. Treatment with TGF-beta1 did not increase the CI significantly, whereas Nandrolone treatment resulted in significant increase in the CI on days 45 and 60. The plasma Ca levels showed slight but gradual increase from day 0 to 60 in almost all groups. Subsequently also, there was no marked change at different intervals in groups A and B; however, significant reduction in plasma Ca was noticed in group C on 15(th) day and in group D on 60(th) day after initiation of treatment. Plasma IP levels in groups B and C showed a decreasing trend up to day 60. After discontinuation of Ca-vit.D3 supplementation, in group B, it further decreased to remain significantly lower on 15(th) day, and in groups C and D, it increased significantly on 60(th) post-treatment day. There was no significant change in the AP activity dur

Topics: Alkaline Phosphatase; Anabolic Agents; Animals; Body Weight; Bone Diseases, Metabolic; Calcium; Cholecalciferol; Female; Male; Nandrolone; Nandrolone Decanoate; Osteocalcin; Parathyroid Hormone; Phosphorus; Rabbits; Random Allocation; Transforming Growth Factor beta1

Hypervitaminosis vitamin D(3) has been recently implicated in premature aging through the regulation of 1alpha hydroxylase expression by klotho and fibroblast growth factor-23 (Fgf-23). Here we examined whether the lack of hormonal function of vitamin D(3) in mice is linked to aging phenomena. For this, we used vitamin D(3) receptor (VDR) "Tokyo" knockout (KO) mice (fed with a special rescue diet) and analyzed their growth, skin and cerebellar morphology, as well as overall motor performance. We also studied the expression of aging-related genes, such as Fgf-23, nuclear factor kappaB (NF-kappaB), p53, insulin like growth factor 1 (IGF1) and IGF1 receptor (IGF1R), in liver, as well as klotho in liver, kidney and prostate tissues. Overall, VDR KO mice showed several aging related phenotypes, including poorer survival, early alopecia, thickened skin, enlarged sebaceous glands and development of epidermal cysts. There was no difference either in the structure of cerebellum or in the number of Purkinje cells. Unlike the wildtype controls, VDR KO mice lose their ability to swim after 6 months of age. Expression of all the genes was lower in old VDR KO mice, but only NF-kappaB, Fgf-23, p53 and IGF1R were significantly lower. Since the phenotype of aged VDR knockout mice is similar to mouse models with hypervitaminosis D(3), our study suggests that VDR genetic ablation promotes premature aging in mice, and that vitamin D(3) homeostasis regulates physiological aging.

Topics: Aging, Premature; Animals; Body Weight; Cerebellum; Cholecalciferol; Female; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Glucuronidase; Humans; Insulin-Like Growth Factor I; Klotho Proteins; Male; Mice; Mice, Knockout; NF-kappa B; Phenotype; Receptor, IGF Type 1; Receptors, Calcitriol; Skin; Survival Rate; Swimming; Tumor Suppressor Protein p53

1alpha,25-dihydroxyvitamin D3 and its analogue, Seocalcitol (EB1089), are able to reverse or slow the process of carcinogenesis in experimental models and cell cultures. The aim of this study was to investigate the effect of administration vitamin D or Seocalcitol to female Sprague-Dawley rats with 1-methyl-1-nitrosourea (MNU)-induced carcinogenesis of mammary glands on binding characteristics and mRNA levels of thyroid hormone receptors (TRs). Chemopreventive administration of vitamin D caused significant reduction of animal body weight. The expression of TRalpha mRNA was significantly higher in liver of animals treated with vitamin D after detection of first tumour. In our experiment, administration of vitamin D or Seocalcitol significantly reduced KA (group MNU+Seo; MNU+D) and increased Bmax (group MNU+Seo) of thyroid receptors in liver when compared to healthy animals. We show that the activity type I 5'-deiodinase was significantly decreased in livers of animals treated with vitamin D. The data from our in vivo experiment has clearly shown, for the first time, that vitamin D but not Seocalcitol i) may affect the body weight of animals, ii) can cause an increase in the expression of TRalpha in rat liver, remaining the functionality of the TRs unaffected, and iii) is responsible for type I iodothyronine 5'-deiodinase activity decrease in rat liver, remaining the expression of the enzyme unaffected.

Topics: Animals; Body Weight; Breast Neoplasms; Calcitriol; Cholecalciferol; DNA; Female; Gene Expression Regulation; Iodide Peroxidase; Liver; Methylnitrosourea; Organ Size; Rats; Rats, Sprague-Dawley; RNA, Messenger; Thyroid Hormone Receptors alpha

Both epidemiological and experimental findings have indicated that components of Western diets influence colonic tumorigenesis. Among dietary constituents, calcium and cholecalciferol have emerged as promising chemopreventive agents. We have demonstrated that a Western-style diet (WD) with low levels of calcium and cholecalciferol and high levels of (n-6) PUFA, increased the incidence of neoplasia in mouse intestine compared with a standard AIN-76A diet; models included wild-type mice and mice with targeted mutations. In the present study, adenomatous polyposis coli (Apc)(1638N/+) mice carrying a heterozygous Apc mutation were fed either an AIN-76A diet, a WD, or a WD supplemented with calcium and cholecalciferol (WD/Ca/VitD3). Diets were fed for 24 wk and effects on cellular and molecular events were assessed by performing immunohistochemistry in colonic epithelium along the crypt-to-surface continuum. Feeding WD to Apc(1638N/+) mice not only enhanced cyclin D1 expression in colonic epithelium compared with AIN-76A treatment as previously reported but also significantly increased the expression of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) concomitantly with a decrease in the proapoptotic Bcl2-associated X protein and the number of apoptotic epithelial cells. WD treatment enhanced mutant Apc-driven small intestinal carcinogenesis and also resulted in the formation of a small number of colonic adenomas (0.16 +/- 0.09; P < 0.05). By contrast, the WD/Ca/VitD3 diet reversed WD-induced growth, promoting changes in colonic epithelium. Importantly, Apc(1638N/+) mice fed the WD/Ca/VitD3 diet did not develop colonic tumors, further indicating that dietary calcium and cholecalciferol have a key role in the chemoprevention of colorectal neoplasia in this mouse model of human colon cancer.

Topics: Adenomatous Polyposis Coli; Adenomatous Polyposis Coli Protein; Animals; Apoptosis; bcl-2-Associated X Protein; Body Weight; Calcium, Dietary; Carcinogenicity Tests; Cholecalciferol; Colon; Cyclin D1; Diet; Disease Models, Animal; Female; Gene Expression Regulation, Neoplastic; Male; Mice; Mutation; Proto-Oncogene Proteins c-bcl-2; Random Allocation

The literature describing vitamin D content of fat tissue is extremely limited. We conducted a pilot study that measured the concentrations of vitamin D(3) in the fat tissue and serum of obese adults. These measurements were performed using a new liquid chromatography mass spectrometry (LC/MS) method. The objectives of this study were: to measure and report the vitamin D(3) concentration in serum and subcutaneous fat samples from obese individuals and to examine the association of vitamin D(3) in fat with vitamin D(3) in serum. This cross-sectional study was conducted in 17 obese men and women who were scheduled to undergo gastric bypass surgery. The mean vitamin D(3) concentration in subjects' subcutaneous fat tissue samples was 102.8 +/- 42.0 nmol/kg. The mean vitamin D(3) concentration in serum was 7.78 +/- 3.99 nmol/l. Vitamin D(3) concentrations of fat tissue and serum were positively correlated (r = 0.68, P = 0.003). Consistent with previous findings in obese subjects, subjects in this study had suboptimal vitamin D status as demonstrated by a mean 25-hydroxyvitamin D concentration of 43.3 +/- 15.4 nmol/l. In conclusion, fat tissue vitamin D(3) can be measured by LC/MS and is detectable in obese subjects with suboptimal vitamin D status. Compatible with the long-standing concept that fat tissue is a storage site for vitamin D, fat tissue and serum vitamin D(3) concentrations were positively correlated.

Topics: Adult; Body Weight; Cholecalciferol; Chromatography, Liquid; Cross-Sectional Studies; Feasibility Studies; Female; Humans; Male; Mass Spectrometry; Middle Aged; Obesity, Morbid; Subcutaneous Fat; Vitamin D Deficiency

In food databases, the specific contents of vitamin D3 and 25-hydroxyvitamin D3 in food have been implemented in the last 10 years. No consensus has yet been established on the relative activity between the components. Therefore, the objective of the present study was to assess the relative activity of 25-hydroxyvitamin D3 compared to vitamin D3. The design was a parallel study in pigs (n 24), which from an age of 12 weeks until slaughter 11 weeks later were fed approximately 55 microg vitamin D/d, as vitamin D3, in a mixture of vitamin D3 and 25-hydroxyvitamin D3, or 25-hydroxyvitamin D3. The end-points measured were plasma 25-hydroxyvitamin D3, and in the liver and loin the content of vitamin D3 and 25-hydroxyvitamin D3. Vitamin D3 and 25-hydroxyvitamin D3 in the feed did not affect 25-hydroxyvitamin D3 in the plasma, liver or loin differently, while a significant effect was shown on vitamin D3 in the liver and loin (P < 0.001). 25-Hydroxyvitamin D3 in the plasma, liver and loin significantly correlates with the sum of vitamin D3 and 25-hydroxyvitamin D3 in the feed (P < 0.05). Therefore, 25-hydroxyvitamin D3 should be regarded as having the same activity as vitamin D3 in food databases. Sole use of 25-hydroxyvitamin D3 as a vitamin D source in pig feed will produce liver and meat with a negligible content of vitamin D3, while an increased content of vitamin D3 in the feed will produce liver and meat with increased content of both vitamin D3 and 25-hydroxyvitamin D3.

Topics: Aging; Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Body Weight; Calcifediol; Cholecalciferol; Liver; Meat; Models, Animal; Subcutaneous Fat; Sus scrofa; Vitamin D

Inactivating mutations of the PHEX (phosphate-regulating gene with homologies to endopeptidases on the X chromosome) endopeptidase, the disease-causing gene in X-linked hypophosphatemia (XLH), results in increased circulating levels of fibroblastic growth factor-23 (FGF23), a bone-derived phosphaturic factor. To determine the causal role of FGF23 in XLH, we generated a combined Fgf23-deficient enhanced green fluorescent protein (eGFP) reporter and Phex-deficient Hyp mouse model (Fgf23(+/-)/Hyp). eGFP expression was expressed in osteocytes embedded in bone that exhibited marked upregulation of eGFP in response to Phex deficiency and in CD31-positive cells in bone marrow venules that expressed low eGFP levels independently of Phex. In bone marrow stromal cells (BMSCs) derived from Fgf23(-/-)/Hyp mice, eGFP expression was also selectively increased in osteocyte-like cells within mineralization nodules and detected in low levels in CD31-positive cells. Surprisingly, eGFP expression was not increased in cell surface osteoblasts, indicating that Phex deficiency is necessary but not sufficient for increased Fgf23 expression in the osteoblast lineage. Additional factors, associated with either osteocyte differentiation and/or extracellular matrix, are necessary for Phex deficiency to stimulate Fgf23 gene transcription in bone. Regardless, the deletion of Fgf23 from Hyp mice reversed the hypophosphatemia, abnormal 1,25(OH)(2)D(3) levels, rickets, and osteomalacia associated with Phex deficiency. These results suggest that Fgf23 acts downstream of Phex to cause both the renal and bone phenotypes in Hyp mice.

Topics: Animals; Body Weight; Bone Density; Bone Marrow Cells; Calcium; Cholecalciferol; Disease Models, Animal; Female; Femur; Fibroblast Growth Factor-23; Fibroblast Growth Factors; Gene Expression Regulation; Green Fluorescent Proteins; Hypophosphatemia, Familial; Male; Membrane Glycoproteins; Metalloendopeptidases; Mice; Mice, Inbred C57BL; Mice, Knockout; Microscopy, Fluorescence; Osteocytes; Parathyroid Hormone; PHEX Phosphate Regulating Neutral Endopeptidase; Phosphorus; Promoter Regions, Genetic

Although several studies have reported a positive effect of n-3 essential fatty acids (EFAs) on bone density post-ovariectomy, the role of specific EFAs has yet to be fully elucidated. In this study, ovariectomised (OVX) rats were supplemented with 0.1 g (LOW) or 1.0 g (HIGH) of eicosapentaenoic acid (EPA)/kg body weight for 9 weeks. Bone mineral density (BMD), 25-hydroxyvitamin D(3) and plasma fatty acid profile were compared to those of OVX and sham animals fed a non-supplemented diet. BMD decreased significantly in all OVX (P<0.001) but not sham rats. There was no difference in BMD between the LOW group and OVX controls. BMD was significantly lower in the HIGH group compared to OVX and sham controls. 25-hydroxyvitamin D(3) levels were significantly higher in both the LOW and HIGH groups compared to OVX controls (P=0.0006 and 0.02, respectively). In conclusion, high-dose EPA supplementation exacerbated the effects of ovariectomy on BMD.

Topics: Animals; Body Weight; Bone and Bones; Bone Density; Cholecalciferol; Eicosapentaenoic Acid; Female; Lipids; Organ Size; Ovariectomy; Radiography; Rats; Uterus

Higher concentrations of Ca in the diet may decrease phytate-phosphorus hydrolysis because of chelation of Ca with the phytin molecule. In experiment 1, drakes were fed 0.74, 0.85, 0.95, or 1.11% Ca (analyzed) from 7 to 18 d of age (6 birds/cage, 8 cages/diet). Intestinal mucosa was collected at 18 d of age from birds fed 0.74 and 1.11% Ca for determination of intestinal phytase activity. In experiment 1, 17 d BW gain and feed consumption exhibited a quadratic response to increasing concentrations of Ca and were found to be maximal for ducks fed the 0.95% Ca diet. Toe ash percentage (18 d) had a quadratic response to increasing concentrations of Ca with a maximal response for birds fed the 0.85% Ca diet. Increasing dietary Ca did not affect P retention from 15 to 17 d of age or intestinal phytase activity and brush border vesicle Ca concentration. A positive correlation was found between the Vmax and the Ca concentration within the vesicles (r = 0.59, P < 0.02), suggesting that the vesicle Ca concentration did not negatively affect the kinetics of the phytase assay. In experiment 2, drakes were fed 0.6, 0.8, 1.0, or 1.2% Ca (formulated) with 826 or 8,260 ICU/kg of vitamin D3 from 0 to 13 d of age. There was no response to increasing concentrations of Ca for performance characteristics or bone ash measurements.

Topics: 6-Phytase; Animal Feed; Animals; Body Weight; Bone and Bones; Calcium; Calcium, Dietary; Cholecalciferol; Dose-Response Relationship, Drug; Ducks; Intestine, Small; Male; Phosphorus

Vitamin D might have an influence on glucose concentrations, due to the presence of VDR receptors on the pancreas. We established an experimental model of type 2 diabetes in spontaneously hypertensive rats (SHR) and Wistar rats in order to investigate the glycemic response.. SHR males (n=6) and Wistar rats (n=6) weighing approximately 89+/-5.5 g and 123.5+/-6.5 g, respectively, after 7 days of basal period, had the chow pattern substituted (350 kcal/100 g) for a hypercaloric/hyperlipidic (HC/HL) diet (490 kcal/100g) and then injected with 40 mg/kg (SHR) and 20 mg/kg (Wistar) streptozotocin I.P. After the creation of diabetes, the rats suffered daily gavage of cholecalciferol (12.5 microg/kg(-) (1)) for 14 days. The blood glucose was assessed twice a week with a glucometer. The data were analyzed by ANOVA.. SHR and Wistar rats fed on a HC/HL diet gained 60 g and 32 g in once week, vs. the basal period, where they only gained 23 g and 13 g, respectively. The cholecalciferol supplementation did not change the glucose concentration in all of the SHR animals. About 40% of the group responded by treatment with reduction of about 60% in glucose concentrations. We did find a 40% of the blood glucose levels in all Wistar rats.. Cholecalciferol is able to reduce blood glucose in this experimental diabetes model.

Topics: Animals; Blood Glucose; Body Weight; Cholecalciferol; Diabetes Mellitus, Type 2; Dietary Supplements; Disease Models, Animal; Male; Rats; Rats, Inbred SHR; Rats, Wistar; Streptozocin

Independent use of K(2) and D(3) and simultaneous application of K(2) and D(3) inhibited the development of osteoporosis caused by PD food intake. The ALP activity of urine as a marker of bone formation osteoporosis did not rise in rats fed PD foods containing D(3), K(2) or both together. Body and womb weights fell in rats fed PD foods with D(3) K(2) and both D(3), K(2). Osteoporosis caused by PD food intake found to be very similar to type II osteoporosis in respects of inhibition by D(3) and K(2) and rising urinary ALP activity.

Topics: Alkaline Phosphatase; Animals; Body Weight; Bone Density; Cholecalciferol; Diet, Protein-Restricted; Female; Osteoporosis; Rats; Rats, Wistar; Vitamin K 2

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Body Weight; Calcium, Dietary; Chickens; Cholecalciferol; Dietary Supplements; Male; Phosphorus, Dietary; Random Allocation; Tibia

1. Two experiments were carried out to investigate responses in performance and bone compositional and structural characteristics in broilers fed diets containing 4 concentrations of vitamin D3 (5, 20, 125 and 250 microg cholecalciferol/kg) at different concentrations of calcium, available phosphorus and vitamin A. 2. In experiment 1, body weight and tibia breaking strength were maximised at 14d with 250 microg vitamin D3/kg, tibia ash was maximised with 125 microg vitamin D3/kg. A high incidence of tibial dyschondroplasia (TD) was decreased to very low levels with 125 microg vitamin D/kg. 3. At 42d, performance and bone characteristics showed no response to vitamin D3 concentrations above 20 microg/kg. 4. Dietary vitamin A within the range 2-4 to 4.5 mg retinol/kg did not show any interaction with vitamin D3 status at either age. 5. In experiment 2, responses to vitamin D3 were strongly influenced by dietary calcium/available phosphorus. With 13 g calcium and 5 g available phosphorus/kg, performance and bone characteristics responded to vitamin D3 concentrations up to 125 microg/kg but more was needed at less optimal concentrations of calcium and available phosphorus. TD incidence was minimised with 250 microg/kg. 6. This study shows that high dietary concentrations of vitamin D3 can prevent TD. It is concluded that the vitamin D3 requirement of broilers up to 14 d of age at optimal dietary calcium and available phosphorus concentrations may be in the range 35 to 50 microg/kg for cortical bone quality and up to 250 microg/kg for prevention of TD. The vitamin D3 requirement for cortical bone quality after 14 d is not higher than 20 microg/kg. These requirements are much higher than earlier estimates and may be related to higher calcium requirements of modern broiler genotypes. Current regulations limiting maximum vitamin D3 concentrations in broiler starter diets may need to be reviewed.

Topics: Animals; Biomechanical Phenomena; Body Weight; Bone and Bones; Calcium, Dietary; Chickens; Cholecalciferol; Diet; Drug Interactions; Growth Plate; Male; Minerals; Nutritional Requirements; Organ Size; Osteochondrodysplasias; Phosphorus, Dietary; Poultry Diseases; Tibia; Vitamin A

The question of whether iron deficiency has direct adverse effects on vertebral trabecular bone and long bones was answered by this study. Four groups of female weanling rats were fed for 5 wk diets that were 1) control; 2) calcium restricted, 1.0 g Ca/kg diet; 3) iron deficient, <8 mg Fe/kg diet; or 4) control, pair-fed to the iron-deficient group. Whole body and femur DEXA analysis revealed that calcium-restricted and iron-deficient rats had lower bone mineral density (BMD) and content (BMC) than pair-fed and control rats. However, pair-fed rats also had decreased BMD and BMC compared to control rats. The third lumbar trabecular bone microarchitecture in both diet-restricted groups had decreased bone volume fraction (BV/TV) and trabecular number and thickness, a less favorable structural model index, and increased trabecular separation compared with the controls and the pair-fed groups as determined by microcomputer tomography. The control and pair-fed groups did not differ from one another, suggesting that iron deficiency and calcium restriction affected vertebrae independently of food intake and body weight. Finite element analysis revealed lower force to compress the vertebrae and lower stiffness but greater von Mises stress in calcium-restricted and iron-deficient groups compared to the control and pair-fed groups. Urinary deoxypyridinium crosslinks, serum osteocalcin, and cholcalciferol were increased in calcium-restricted rats compared to the other 3 groups. Using micro-CT imaging technology, this study demonstrated microarchitectural pathology due to iron deficiency upon vertebral trabecular bone compared to the control and pair-fed rats, although not to the same extent as severe calcium restriction.

Topics: Absorptiometry, Photon; Animals; Body Weight; Bone and Bones; Bone Density; Cholecalciferol; Energy Intake; Female; Femur; Iron Deficiencies; Osteocalcin; Pyridines; Rats; Rats, Long-Evans; Spine; Tomography, X-Ray Computed

In the first oftwo experiments, 123 calf-fed steers were used over a 2-yr period to evaluate the effects of trenbolone acetate (TBA)-based implants administered alone or in combination with zeranol implants on fresh beef muscle quality, color, and physiological maturity of the carcass. Implant treatments decreased (P < 0.05) a* values (d 0 and d 3 of retail display) and b* values (d 0, d 1, and d 3 of retail display) after 14 d of aging. Carcasses from cattle initially implanted with Revalor-S and reimplanted with Revalor-S on d 60 of the finishing period showed increased lean and bone maturity scores and ash content of the 9th to 11th thoracic buttons and Warner-Bratzler shear force values (WBS) compared to those initially implanted with Ralgro and subsequently reimplanted with Revalor-S or control cattle. In addition, implants decreased (P < 0.05) marbling, percentage of the carcasses grading Choice, and kidney, pelvic, and heart fat (KPH). Implant treatments increased (P < 0.05) ADG, hot carcass weights, and longissimus muscle (LM) area. In the second experiment over a 2-yr period, 166 steers fed as yearlings were allotted to one of two implant treatments and one of two vitamin D3 preharvest supplementation treatments. Implanted steers had heavier (P < 0.05) final body weights and higher (P < 0.05) ADG, less (P < 0.05) KPH fat, and larger (P < 0.05) LM. Also, implanted steers had more (P < 0.05) advanced bone maturity scores, higher (P < 0.05) ash content of the 9th to 11th thoracic buttons, and higher (P < 0.05) WBS values on 5-d postmortem loin steaks. Vitamin D3 feeding decreased (P < 0.05) final live weight, ADG (P < 0.05), and LM (P < 0.05), but did not significantly improve WBS values. In Experiment 2, neither implant treatment nor vitamin D3 supplementation had significant effects on L*, a*, or b* values of muscles in steaks before or during simulated retail display.

Topics: Administration, Oral; Anabolic Agents; Animals; Body Composition; Body Weight; Cattle; Cholecalciferol; Drug Combinations; Drug Implants; Estradiol; Estrogens, Non-Steroidal; Male; Meat; Pigmentation; Random Allocation; Trenbolone Acetate; Zeranol

Fetal mineralization appears to be driven by the pregnancy-induced stimulation of intestinal Ca absorption. We thus hypothesized that mineralization would be impaired in fetuses of mice that lack the vitamin D receptor (VDR). Here we report on the maternal response to pregnancy, and the fetal mineralization, in mice with a homozygous disruption of the VDR gene (VDR-/-) mated with wild-type (wt) males. We found that VDR-/- mice show mild hypocalcemia, clear rickets and osteomalacia on bone histomorphometry, lower cortical bone density on quantitative tomography, and reduced concentrations of calbindin-D9k (CaBP-D9k) in duodenal mucosa and kidney. The skeletal response to pregnancy was comparable in wt and VDR-/- mice; duodenal CaBP-D9k concentrations increased during pregnancy in VDR-/- as in wt mice, but remained 40% lower than in wt mice. We confirmed our hypothesis that mineralization is defective in d18.5 VDR+/- fetuses of VDR-/- mice, both by whole-body Ca determination and histomorphometric evaluation; the number of osteoclastic cells in bone was increased. The fetuses were hypercalcemic and had a 5-fold increase in circulating 1,25(OH)2D3. We then studied pregnancies in VDR-/- females, mated with wt males, fed a high Ca/P/lactose rescue diet during pregnancy. The rescue diet normalized the mineralization, the number of osteoclastic cells, and plasma Ca and 1,25(OH)2D3 concentrations in the fetuses. We interpret the data as evidence that, to ensure normal fetal mineralization, the maternal VDR-dependent intestinal Ca absorption can be substituted by passive Ca absorption entrained by a higher Ca intake. Alternatively or additionally, elevated 1,25(OH)2D3 in utero may disturb bone development.

Topics: Animals; Body Weight; Bone and Bones; Calbindins; Calcification, Physiologic; Calcium; Cholecalciferol; Dietary Supplements; Duodenum; Female; Fetus; Kidney; Male; Mice; Mice, Knockout; Phenotype; Placenta; Pregnancy; Pregnancy, Animal; Receptors, Calcitriol; S100 Calcium Binding Protein G

1. A series of 5 trials was conducted with Cobb chickens in order to determine the effect of 25-hydroxycholecalciferol (25OHD3) on their performance and bone development under adequate Calcium (Ca) and Phosphorus (P) supplementation, and under moderate dietary restriction of Ca and P. Formulated beadlets of 25OHD3, trade name HY-D (IsoGen, Naperville, IL, USA) were used as the 25OHD3 source. 2. Five to 10 microg of cholecalciferol (vitamin D3) or 25OHD3/kg diet were sufficient to ensure normal body weight (BW) and bone ash in chickens under continuous lighting. The two materials had similar effects on BW and bone ash. 3. In one out of the three experiments, 25OHD3 increased BW and BW gain, while in the others it had a similar effect to that of vitamin D3, or even a slight negative effect in a trial conducted on the floor, in which the diets were supplemented with the D sources at 75 microg/kg. The effects of both D sources on bone ash and on the severity or frequency of tibial dischondroplasia were similar. 4. 25OHD3 restrained the effect of moderate dietary P restriction, but not of Ca restriction, on BW gain and bone ash in 22-d-old chickens. This effect could not be explained by an higher P bioavailability in the 25OHD3-fed chickens.

Topics: Animal Feed; Animals; Biological Availability; Body Weight; Bone and Bones; Bone Development; Calcifediol; Calcium; Calcium, Dietary; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Male; Minerals; Phosphorus, Dietary; Random Allocation; Weight Gain

Phosphate utilization by fish is an important issue because of its critical roles in fish growth and aquatic environmental pollution. High dietary phosphorus (P) levels typically decrease the efficiency of P utilization, thereby increasing the amount of P excreted as metabolic waste in effluents emanating from rainbow trout aquaculture. In mammals, vitamin D3 is a known regulator of P utilization but in fish, its regulatory role is unclear. Moreover, the effects of dietary P and vitamin D3 on expression of enzymatic and transport systems potentially involved in phosphate utilization are little known. We therefore monitored production of effluent P, levels of plasma vitamin D3 metabolites, as well as expression of phosphatases and the sodium phosphate cotransporter (NaPi2) in trout fed semipu diets that varied in dietary P and vitamin D3 levels. Mean soluble P concentrations varied markedly with dietary P but not with vitamin D3, and constituted 40-70% of total effluent P production by trout. Particulate P concentrations accounted for 25-50% of effluent P production, but did not vary with dietary P or vitamin D3. P in settleable wastes accounted for <10% of effluent P. The stronger effect of dietary P on effluent P levels is paralleled by its striking effects on phosphatases and NaPi2. The mRNA abundance of the intestinal and renal sodium phosphate transporters increased in fish fed low dietary P; vitamin D3 had no effect. Low-P diets reduced plasma phosphate concentrations. Intracellular phytase activity increased but brushborder alkaline phosphatase activity decreased in the intestine, pyloric caeca, and gills of trout fed diets containing low dietary P. Vitamin D3 had no effect on enzyme activities. Moreover, plasma concentrations of 25-hydroxyvitamin D3 and of 1,25-dihydroxyvitamin D3 were unaffected by dietary P and vitamin D3 levels. The major regulator of P metabolism, and ultimately of levels of P in the effluent from trout culture, is dietary P.

Topics: 6-Phytase; Alkaline Phosphatase; Analysis of Variance; Animals; Aquaculture; Blotting, Western; Body Composition; Body Weight; Calcifediol; Calcitriol; Cholecalciferol; Circadian Rhythm; Feces; Gastrointestinal Contents; Gene Expression Regulation; Gills; Intestinal Mucosa; Intestines; Kidney; Microvilli; Muscles; Oncorhynchus mykiss; Phosphates; Phosphoric Monoester Hydrolases; Phosphorus; Phosphorus, Dietary; RNA, Messenger; Sodium-Phosphate Cotransporter Proteins; Symporters

Time-dependent differences in adverse reactions and efficacy by a repeated administration of 1,25(OH)2 vitamin D3 (vit D, 0.3 microg/Kg/day for 12 weeks) were examined in 5/6 nephrectomized rats under a condition of 12-hour light-dark cycle. The 5/6 nephrectomy increased serum concentrations of phosphate, osteocalcin and PTH, and urinary excretions of phosphate and deoxypyridinoline (DPD) while the maneuver reduced serum Ca concentration and its urinary excretion. Animals with a dosing of the drug at 2 hours after light on (HALO) had more grade of hypercalcemia and hyperphosphatemia than those at 14 HALO. Reduction of serum intact PTH and increase of serum vit D were observed in both groups with a similar extent. Increase of osteocalcin by the drug was greater in 14 HALO trial. Urinary excretion of DPD was not influenced by the treatment. The increase in bone density of femur was greater in 14 HALO than in 2 HALO trials. These results suggest that adverse reactions of vit D were ameliorated and its efficacy was enhanced after the repeated dosing of the drug at 14 HALO. Time-dependent variation in the sensitivity of the drug to osteoblast was involved in the mechanism of these events, while the roles of pharmacokinetic alteration and renal response were small, if any.

Topics: Amino Acids; Animals; Biomarkers; Body Weight; Bone Density; Calcium; Cholecalciferol; Creatinine; Male; Nephrectomy; Osteocalcin; Parathyroid Hormone; Phosphorus; Rats; Rats, Wistar; Time Factors

Studies were conducted to determine the effect of dietary supplementation with cholecalciferol (D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], 1alpha-hydroxycholecalciferol (1alpha-OHD3), and 25-hydroxycholecalciferol (25-OHD3) on utilization of phytate P by broiler chickens. Three experiments were conducted with corn-soybean meal type diets with D3 and 1,25-(OH)2D3 being tested in one experiment and 1,25-(OH)2D3, 1alpha-OHD3, and 25-OHD3 being tested in two experiments of exactly the same design. In the first experiment, high levels of D3 (110 microg and 220 microg/kg of diet) increased phytate P utilization, but the increase was not as great as that obtained from 1,25-(OH)2D3 supplementation. In the other two experiments, 1,25-(OH)2D3, D3 and 1alpha-OHD3 were consistently effective in increasing phytate P utilization as measured by plasma Ca and P, incidence of P rickets, bone ash, and retention of Ca, P, and phytate P. Supplementation with 25-OHD3 in general gave smaller and more inconsistent responses to these criteria, indicating some inconsistency in its ability to improve phytate P utilization.

Topics: Animal Nutritional Physiological Phenomena; Animals; Body Weight; Calcifediol; Calcitriol; Calcium; Chickens; Cholecalciferol; Diet; Dietary Supplements; Glycine max; Hydroxycholecalciferols; Male; Phosphorus; Phytic Acid; Zea mays

Plasma concentrations of the main vitamin D(3) metabolites (i.e., 25(OH)D(3), 1,25(OH)(2)D(3), and 24,25(OH)(2)D(3)) were measured in 14 weeks old large- and small-breed dogs (adult body weight 60 kg vs. 6 kg), raised under the same conditions. Levels of 25(OH)D(3) (approx. 22 microg/l) and 1,25(OH)(2)D(3) (approx. 40 ng/l) were similar in both groups, whereas plasma 24,25(OH)(2)D(3) concentrations were lower in large-breed dogs (7 microg/l vs. 70 microg/l, large- vs. small-breed dogs, respectively). The lower plasma 24,25(OH)(2)D(3) concentrations could be explained by the higher plasma GH and IGF-I concentrations in the large- vs. small-breed dogs, and these hormones are known to suppress 24-hydroxylation. Plasma 24,25(OH)(2)D(3) concentrations increased during Ca supplementation in small-breed but not in large-breed dogs (100 microg/l vs. 7 microg/l, respectively). Hypophosphatemia induced by a high dietary Ca content was only seen together with increased plasma 1,25(OH)(2)D(3) concentrations in euparathyroid dogs and not in hypoparathyroid dogs. Hyperparathyroidism due to Ca deficiency was accompanied by increased plasma 1,25(OH)(2)D(3) concentrations and decreased plasma 24,25(OH)(2)D(3) concentrations in both large- and small-breed dogs, together with generalized osteoporosis. Large-breed pups fed on a standard diet supplemented with Ca and P had decreased plasma concentrations of both 25(OH)D(3) and 1,25(OH)(2)D(3), which may indicate an increased clearance of these metabolites; the low plasma concentrations of the di-hydroxylated vitamin D metabolites were considered responsible for the disturbance in cartilage maturation (i.e., osteochondrosis) in these dogs. Even lower concentrations of all vitamin D(3) metabolites were seen in young dogs raised on a vitamin D(3)-deficient diet, and led to disturbed osteoid and cartilage mineralization (i.e., rickets). These studies indicate that there is a hierarchy of factors regulating vitamin D(3) metabolism in dogs, i.e., GH and IGF-I suppress 24-hydroxylase more than hypercalcemia or hypophosphatemia does; 1,25(OH)(2)D(3) and 24,25(OH)(2)D(3) are only reciprocally related in hyperparathyroidism; excessive Ca and P intake increases the turnover of vitamin D(3) metabolites; and the synergism between parathyroid hormone and 1,25(OH)D(3) seems to play a role in skeletal mineralization. The low plasma 24,25(OH)(2)D(3) concentrations in large-breed dogs raised on standard dog food may play a role in the etiology

Topics: Animals; Body Weight; Bone Development; Calcium; Cholecalciferol; Diet; Dogs; Growth Hormone; Humans; Insulin-Like Growth Factor I; Parathyroid Hormone; Phosphorus; Radiography; Radius; Ribs; Rickets; Ulna; Vitamin D Deficiency

Both calcium and vitamin D are thought to be able to inhibit colon carcinogenesis. To better define the effects of vitamin D, we studied 1alpha,25-(OH)(2)-D(3) and a noncalcemic synthetic analogue of vitamin D(3) (VD(3)) in the Apc(min) mouse. Female Apc(min) mice 4-5 weeks old were randomized to four groups: a VD(3)-treated group (n = 11) were given injections of 0.01 microg of 1alpha,25-(OH)(2)-D(3) i.p. three times per week; an analogue-treated group (n = 10) received 5 microg of 1alpha,25-(OH)(2)-16-ene-19-nor-24-oxo-D(3) i.p. three times per week; and a control group (n = 12) received sham injections of PBS. A sulindac-treated group (n = 10) was used as a positive control. Doses of these compounds were chosen based on previous toxicity studies in mice and rats. After 10 weeks of treatment, mice were killed and two observers (S. H., R. W. I.), blinded to treatment, scored polyp number and size. Tumor number was not affected with 1alpha,25-(OH)(2)-D(3) or vitamin D analogue administration. A significant decrease in total tumor load (sum of all polyp areas) over the entire gastrointestinal tract was seen in the analogue (36% decrease; P < 0.05) and the VD(3) groups (46%; P < 0.001). There was a significant decrease in polyp number (49%; P < 0.001) and polyp area (70%; P < 0.001) in the sulindac group. Reverse transcription-PCR of the total RNA derived from intestinal tissue revealed expression of the vitamin D receptor throughout the small intestine and the colon. Serum calcium levels in the analogue group were not elevated at week 4 of treatment and only moderately elevated (22%) by week 8 (P < or =0.001). In contrast, serum calcium in the VD(3) group was significantly elevated (P < or =0.001) at weeks 4 (23%) and 8 (45%). Food intake and growth rate were significantly lower in the VD(3) group (26%, P < 0.001, and 27%, P < 0.001, respectively) at week 10. In contrast, food intake and growth rate were similar for the control, sulindac, and analogue groups. Our results indicate that a noncalcemic analogue of vitamin D can significantly decrease intestinal tumor load in Apc(min) mice without severe toxic side effects and suggest that these compounds may have utility as chemopreventive agents in groups at high-risk for colon cancer.

Topics: Adenomatous Polyposis Coli; Animals; Body Weight; Calcitriol; Calcium; Cholecalciferol; Colonic Neoplasms; Eating; Female; Mice; Mice, Inbred C57BL; Receptors, Calcitriol

Two experiments were conducted using a corn-soybean meal diet that meets or exceeds the NRC (1984) requirements for all nutrients except cholecalciferol (D3) to determine the effectiveness of 1-alpha-hydroxycholecalciferol (1alpha-OHD3) as a substitute for D3 in the diet of young broilers. Ross x Ross mixed-sex, 1-d-old chicks were reared in Petersime battery brooders not exposed to ultraviolet light with feed and water supplied ad libitum for 16 d. In Experiment 1, D3 was fed at 0, 2.5, 5, 10, 20, and 40 microg/kg and one source of 1alpha-OHD3-(Hoffmann-LaRoche, Inc.; HLR) was fed at 0.625, 1.25, 2.5, 5, and 10 microg/kg of diet. In Experiment 2, the D3 was fed at 0, 2.5, 5, and 10 microg and two sources of 1alpha-OHD3-[HLR and Majestic Research Inc. (MRI)] were fed at 0, 0.625, 1.25, and 5 microg/kg of diet. Slope ratio analysis of data from the measurement of 16-d body weight, plasma Ca, rickets, and bone ash indicated bioavailability of the 1alpha-OHD3 as compared to D3 from 1.88 to 21.2. Percentage bone ash gave the most precise values in both experiments. Considering all the data from both experiments, the 1alpha-OHD3 appears to be approximately eight times as effective as D3 for satisfying the requirements of several criteria in two experiments with broiler chickens.

Topics: Animal Feed; Animal Nutritional Physiological Phenomena; Animals; Biological Availability; Body Weight; Bone and Bones; Calcium; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Female; Hydroxycholecalciferols; Intestinal Absorption; Male; Minerals; Nutritional Requirements; Poultry Diseases; Rickets

Postnatal mammary gland morphogenesis is achieved through coordination of signaling networks in both the epithelial and stromal cells of the developing gland. While the major proliferative hormones driving pubertal mammary gland development are estrogen and progesterone, studies in transgenic and knockout mice have successfully identified other steroid and peptide hormones that impact on mammary gland development. The vitamin D(3) receptor (VDR), whose ligand 1,25-dihydroxyvitamin D(3) is the biologically active form of vitamin D(3), has been implicated in control of differentiation, cell cycle and apoptosis of mammary cells in culture, but little is known about the physiological relevance of the vitamin D(3) endocrine system in the developing gland. In these studies, we report the expression of the VDR in epithelial cells of the terminal end bud and subtending ducts, in stromal cells and in a subset of lymphocytes within the lymph node. In the terminal end bud, a distinct gradient of VDR expression is observed, with weak VDR staining in proliferative populations and strong VDR staining in differentiated populations. The role of the VDR in ductal morphogenesis was examined in Vdr knockout mice fed high dietary Ca(2+) which normalizes fertility, serum estrogen and neonatal growth. Our results indicate that mammary glands from virgin Vdr knockout mice are heavier and exhibit enhanced growth, as evidenced by higher numbers of terminal end buds, greater ductal outgrowth and enhanced secondary branch points, compared with glands from age- and weight-matched wild-type mice. In addition, glands from Vdr knockout mice exhibit enhanced growth in response to exogenous estrogen and progesterone, both in vivo and in organ culture, compared with glands from wild-type mice. Our data provide the first in vivo evidence that 1,25-dihydroxyvitamin D(3) and the VDR impact on ductal elongation and branching morphogenesis during pubertal development of the mammary gland. Collectively, these results suggest that the vitamin D(3) signaling pathway participates in negative growth regulation of the mammary gland.

Topics: Animals; Apoptosis; Body Weight; Calcitriol; Calcium; Cell Division; Cholecalciferol; Female; Fertility; Male; Mammary Glands, Animal; Mice; Mice, Knockout; Organ Culture Techniques; Progesterone; Receptors, Calcitriol

We attempted to provide experimental evidence linking increased dietary calcium to progression of prostate cancer, as suggested by some epidemiological studies, using a heterotopic prostate cancer nude mice model.. Twenty heterotopic LNCaP prostate cancer tumor bearing nude mice were randomly assigned to one of the four groups: (I) high fat/low calcium diet, (II) high fat and high calcium diet, (III) high fat diet fortified with Vitamin D3, and (IV) high fat and high calcium diet fortified with Vitamin D3. In addition to weekly animal weights and tumor size measurements, the serum prostate specific antigen (PSA), 25-hydroxy Vitamin D3, calcium, phosphorus, total protein, albumin (to account for bound calcium) [1], and serum alkaline phosphatase (a measure of bone loss) [2] were determined at the termination of experiments.. Although the serum calcium and 25-hydroxy Vitamin D3 were significantly higher in groups III and IV compared to groups I and II (P < 0.05), there was no significant difference between the tumor growth rates, final tumor weights (P = 0.9), and the serum PSA levels (P = 0.94) between the four groups.. The results suggest that dietary calcium does not significantly affect the growth of heterotopic LNCaP prostate cancer in nude mice.

Topics: Adenocarcinoma; Alkaline Phosphatase; Animals; Blood Proteins; Body Weight; Calcifediol; Calcium; Calcium, Dietary; Cell Division; Cholecalciferol; Dietary Fats; Disease Progression; Humans; Male; Mice; Mice, Nude; Neoplasms, Hormone-Dependent; Phosphorus; Prostate-Specific Antigen; Prostatic Neoplasms; Random Allocation; Serum Albumin

We used a split-plot design of five diets: control (corn-soy) with 3.8% Ca, 10% flaxseed with 3.8% Ca, 10% flaxseed with 4.5% Ca, 10% flaxseed with 3.8% Ca and 22,000 IU vitamin D3/kg, and 10% flaxseed with 4.5% Ca and 22,000 IU vitamin D3/kg, and two strains of birds, DeKalb Delta (DD) and Hy-Line W-36 (HL), to evaluate long-term effects of flaxseed supplementation on egg production parameters. Each of the five treatments was randomly assigned and replicated six times with five hens per replicate pen from 21 to 57 wk of age. Phase I was from 21 to 39 wk, Phase II was from 40 to 48 wk, and Phase III was from 49 to 57 wk. Feed consumption was significantly (P < 0.04) greater for the hens fed 10% flaxseed diets (100.9 g) when compared to the corn-soy controls (99.3 g). Overall average egg production (P < 0.05) was 87.8, 87.1, 86.0, 87.1, 84.8, for diets 1, 2, 3, 4, and 5, respectively. Average hen weights during the study were significantly lower for the flaxseed-fed hens (1.559 kg) compared to the controls (1.616 kg). Egg weight was significantly affected by diet during Phase III with heavier eggs from flaxseed fed hens (62.6 g) compared to controls (61.44 g), but overall egg weight was not significantly affected. Average egg mass was not significantly affected by dietary treatments, but DD hens had a decrease in egg mass with Ca supplementation (Diet 2 vs. Diet 3), whereas HL egg mass increased with Ca supplementation. Percentage albumen had a significant strain effect and strain by diet interactions. Overall, significantly less albumen (P < 0.001) was produced by HL (59.4%) compared to DD (61.3%). Supplemental Ca increased albumen percentage in DD (interaction effect P < 0.03) and decreased albumen percentage in the HL strain. Flaxseed supplementation significantly increased albumen percentage (P < 0.02) when compared to the corn-soy control, 60.5 and 59.9%, respectively. An interaction effect (P < 0.01) was noted for percentage wet yolk, in which increasing Ca decreased wet yolk percentage in DD but increased yolk percentage in HL. Wet yolk percentage was also significantly (P < 0.001) less in DD (25.0%) when compared to HL (26.9%). Addition of flaxseed decreased yolk percent when compared to controls (P < 0.03) during Phase II. Ca supplementation significantly (P < 0.03) increased yolk solids in both strains. Grams of yolk solids per egg were affected by flaxseed supplementation (P < 0.06). Flaxseed eggs contained 7.18 g per egg yolk solids compared to

Topics: Age Factors; Animals; Body Weight; Calcium, Dietary; Chickens; Cholecalciferol; Egg Shell; Egg Yolk; Eggs; Female; Flax; Longitudinal Studies; Ovalbumin; Oviposition; Random Allocation; Seeds

The chronotherapeutic effects of 1-alpha-(OH) vitamin D3, a pro-drug of 1,25(OH)2 vitamin D3 (1,25(OH)2D3), were evaluated by repeated dosing of the drug in aged stroke-prone spontaneously hypertensive male rats, a model of osteoporosis. Animals (7 months old) were kept in rooms with a 12-h light/dark cycle. Drug (0.5 microg/kg) or vehicle was given once daily at 2 or 14 h after lights on for 3 months. The severity of adverse effects such as body weight loss, hypercalcemia and hyperphosphatemia was significantly less when the drug was given at 14 h after lights on (14 HALO). Serum 1,25(OH)2 vitamin D3 concentrations of 2 h after lights on (2 HALO) group and 14 HALO group did not differ significantly after dosing. The decrease in parathyroid hormone (PTH) level 12 weeks after the start of the study was greater in the 14 HALO group than in the 2 HALO group. Urinary excretion of inorganic Ca and P in the 2 HALO group was greater than that in the 14 HALO group. Urinary excretion of deoxypyridiniline, an index of the bone resorption capacity of osteoclasts, was much suppressed in the 14 HALO group, suggesting that the efficacy of vitamin D3 for suppressing bone resorption might vary with the dosing time. The increase in bone density of both femurs, determined by dual-energy X-ray absorption at the end of the study, was greater in the 14 HALO group than in the 2 HALO group. This is the first study to show the dosing time-dependent efficacy and toxicity of active vitamin D3 in an animal model of osteoporosis. These results indicate that a chronopharmacological approach is beneficial for establishing a more effective and/or safer regimen of active vitamin D3 for the treatment of osteoporosis.

Topics: Aging; Amino Acids; Animals; Body Weight; Bone Density; Calcium; Cholecalciferol; Chronotherapy; Disease Models, Animal; Hypercalcemia; Hypertension; Male; Osteoporosis; Parathyroid Hormone; Phosphates; Rats; Rats, Inbred SHR; Steroid Hydroxylases; Time Factors; Weight Loss

Research was conducted to determine the effects of supplemental dietary vitamin D3 on DMI, carcass traits, Warner Bratzler shear (WBS) force, calpastatin activity, plasma minerals, pH (0, 3, 12, and 24 h after slaughter), water-holding capacity (WHC), and sensory characteristics of three muscles. Pre-slaughter vitamin D3 treatments included no supplemental vitamin D3, 6 x 106 IU (MIU) of vitamin D3 for 4 d, or 6 MIU of vitamin D3 for 6 d. Cattle were slaughtered and carcasses were chilled for 48 h before removal of steaks from the longissimus, gluteus medius, and biceps femoris muscles. Steaks were aged at 2 degrees C for 7, 14, or 21 d before cooking to a final internal temperature of 70 degrees C for WBS and sensory panel analysis. Dry matter intake was lower for steers supplemented with vitamin D3 for 4 or 6 d. Live and carcass weights were lower (P < 0.05) in steers supplemented with vitamin D3. Supplementing 6 MIU/6 d of vitamin D3 decreased (P < 0.05) WBS values of gluteus steaks (pooled over aging times). Longissimus steaks from steers supplemented with vitamin D3 for 6 d had lower (P < 0.05) WBS force values than these steaks from control steers or steers fed vitamin D3 for 4 d at 7 d postmortem. Biceps femoris steaks from steers receiving vitamin D3 for 4 d had higher WBS values than steaks from control steers at 14 and 21 d postmortem. Feeding vitamin D3 at 6 MIU for 6 d decreased (P < 0.05) the percentage of steaks that had WBS values > or = 3.86 kg for all steaks. Feeding vitamin D3 had no effect on palatability traits evaluated by trained panelists. Blood Ca concentrations were greater (P < 0.05) when vitamin D3 was fed and with increased vitamin D3 feeding time. Feeding vitamin D3 for 6 d (vs 4 d) delayed pH decline for all muscle types after 0, 3, and 12 h postmortem. Water-holding capacity was increased (P > 0.02) after 0 h, 24 h, and 21 d postmortem when vitamin D3 was fed and was greater at 0 and 24 h if vitamin D3 was fed for 6 d rather than 4 d. These data suggest that supplementing 6 MIU of vitamin D3 will decrease DMI and improve beef tenderness through increased blood plasma Ca concentrations and WHC.

Topics: Animals; Body Weight; Calcium; Calcium-Binding Proteins; Cattle; Cholecalciferol; Cysteine Proteinase Inhibitors; Dose-Response Relationship, Drug; Energy Intake; Food Handling; Male; Meat; Muscle, Skeletal; Postmortem Changes; Random Allocation; Taste; Time Factors

This study explores the effects of chronic administration of vitamin D(3) compounds on several biological functions in mice. Knowledge of long-term tolerability of vitamin D(3) analogs may be of interest in view of their potential clinical utility in the management of various pathologies such as malignancies, immunological disorders and bone diseases. Four unique vitamin D(3) analogs (code names, compounds V, EO, LH and LA) and 1,25-dihydroxyvitamin D(3) (1, 25(OH)(2)D(3)) were administered i.p. for 55 weeks to Balb/c mice. Each analog had previously been shown to have potent in vitro activities. After 55 weeks of administration, the mice had a profound decrease in their serum levels of interleukin-2 (IL-2). Likewise, several analogs depressed serum immunoglobulin G concentrations (compounds LH and LA), but levels of blood lymphocytes and splenic lymphocyte subsets (CD4, CD8 and CD19) were not remarkably depressed. The percent of committed myeloid hematopoietic stem cells was 4- to 5-fold elevated in the bone marrow of the mice that received analogs LH and V; nevertheless, their peripheral blood white and red cell counts and platelets were not significantly different in any of the groups. The mice that received 1,25(OH)(2)D(3) had a decrease in bone quantity and quality with a decrease in cross-sectional area and cortical thickness, and a 50% reduction in both stiffness and failure load compared with the control group. In contrast, the cohort that received a fluorinated analog (compound EO) developed bones with significantly larger cross-sectional area and cortical thickness as well as stronger mechanical properties compared with the control group. At the conclusion of the study, body weights were significantly decreased in all experimental mice. Their blood chemistries were normal. Extensive gross and microscopic autopsy analyses of the mice at the conclusion of the study were normal, including those of their kidneys. In conclusion, the vitamin D(3) analogs were fairly well tolerated. They did suppress immunity as measured by serum IL-2 and may provide a means to depress the immune response after organ transplantation and for autoimmune diseases. Use of these analogs prevented the detrimental effects of vitamin D(3) administration on mechanical and geometric properties of bone, while one analog (compound EO) actually enhanced bone properties. These results suggest that long-term clinical trials with the analogs are feasible.

Topics: Animals; Body Weight; Bone and Bones; Cholecalciferol; Drug Tolerance; Hematopoietic Stem Cells; Immunoglobulins; Interleukin-2; Mice; Mice, Inbred BALB C

Male turkeys immunosuppressed by injection with dexamethasone (DEX) were given supplemental vitamin D3 in their drinking water in two experiments. In Experiment 1, vitamin D3 was supplemented at a dosage of either 2,064 IU/kg (low level) or 4,128 IU/kg (high level) in drinking water provided ad libitum only from Days 1 through 5 after hatch. In Experiment 2, vitamin D3 was provided at the low dosage for the first 5 d after hatch, followed by treatment with the high dosage for 12 h before and 12 h after each stressful event, which included weekly weighings and two DEX treatments. In both experiments, at 5 wk of age half of the birds were given intramuscular injections of 2 mg/kg DEX on 3 alternating d. In Experiment 1, 100 cfu of Escherichia coli was inoculated into the left thoracic airsac at the time of the third DEX injection. All mortalities were examined, and 10 birds per pen were necropsied 2 wk after treatment and examined for lesions of airsacculitis and turkey osteomyelitis complex (TOC). Four birds per pen were bled before necropsy, and white blood cell total counts, differential white blood cell counts, and clinical chemistry values were determined. In Experiment 2, healthy surviving birds were grown for an additional 5-wk period, after which the DEX-treated birds were given a second series of DEX injections and were bled and necropsied 2 wk later. There were no significant effects of vitamin D3 treatment in combined general linear models analysis of Experiment 1; however, when birds not treated with DEX or E. coli were compared with those treated with both DEX and E. coli, supplementation with the low level of vitamin D3 significantly decreased TOC incidence. There were no significant effects of vitamin D3 treatment in birds treated with DEX at 5 wk of age in Experiment 2. However, when surviving birds were given a second DEX treatment at 12 wk, vitamin D3 treatment resulted in significantly lower incidence of mortality, TOC, green liver, isolation of bacteria from tissues, and lower airsacculitis scores and heterophil-to-lymphocyte ratios than controls. Vitamin D3 also improved BW, relative weights of the liver and heart, and serum levels of glucose and alanine aminotransferase (ALT) of birds receiving two treatments with DEX. The ability of vitamin D3 supplementation to protect turkeys from the immunosuppressive effects of multiple DEX treatments emphasizes the role of vitamin D3 as a prohormone that affects health and disease resistance in t

Topics: Alanine Transaminase; Alkaline Phosphatase; Animals; Aspartate Aminotransferases; Blood Glucose; Body Weight; Cholecalciferol; Creatine Kinase; Dexamethasone; Escherichia coli; Escherichia coli Infections; Glucocorticoids; Least-Squares Analysis; Leukocyte Count; Linear Models; Liver; Lymphocyte Count; Lymphocyte Subsets; Male; Osteomyelitis; Poultry Diseases; Random Allocation; Stress, Physiological; Turkeys; Uric Acid

Circulating plasma fat-soluble vitamin and mineral concentrations were compared in captive females of three species for fruit bats (Pteropus vampyrus, Pteropus hypomelanus, and Pteropus pumilus) fed the same diet. Daily total food intake averaged 28% of body weight on an as-fed basis or 7% on a dry matter basis. Dietary leftovers contained higher concentrations of phosphorus, magnesium, and zinc than the diet offered, suggesting some nutrient selectivity. Additionally, fecal mineral concentrations were two- to threefold higher than dietary concentrations of corresponding nutrients. Plasma concentrations of vitamin A (0.02-0.05 microg retinol/ml), vitamin D (1.50 ng 25-OH D3/ml; 93-108 pg 1,25 diOH D3/ml), and vitamin E (0.49-1.05 microg alpha-tocopherol/ml) were lower than in other herbivorous mammals, whereas plasma mineral concentrations were within normal mammalian ranges. These data may help assess the nutritional status of fruit bats.

Topics: Animal Nutritional Physiological Phenomena; Animals; Animals, Zoo; Body Weight; Chiroptera; Cholecalciferol; Diet; Energy Intake; Feces; Female; Minerals; Vitamin A; Vitamin D; Vitamin E; Vitamins

The aim of the present work was to gain insight into a putative anticancer effect of dietary vitamin D3 (cholecalciferol) in a rat model of colon carcinogenesis. Male rats were assigned to three different dietary groups. The dietary regimens were based on a standard murine-defined diet (AIN-76A) or a stress diet containing 20% fat, reduced Ca2+ concentration, a high phosphorus-to-Ca2+ ratio, and either low or high vitamin D3 content. Colorectal cancer was induced by administration of the procarcinogen 1,2-dimethylhydrazine (DMH). Blood Ca2+, 1,25-dihydroxyvitamin D3 [1,25(OH)2D3], and 25-hydroxyvitamin D3 [25(OH)D3] levels were measured in DMH-treated rats and in respective weight- and age-matched dietary control groups. Colonic epithelial proliferation was assessed by determining thymidine kinase (TK) activity, bromodeoxyuridine (BrdUrd) incorporation into crypt cell DNA, and the mean labeling index along the colonic crypt continuum. Maintenance of rats on the stress diet either unmodified or supplemented with vitamin D3 in the absence of carcinogen treatment provoked a time-dependent rise in colonic TK activity and hyperproliferation of colonic epithelium. DMH treatment of rats maintained on the standard diet caused a marked increase in the proliferative indexes of colonic epithelium and in expansion of the crypt proliferative compartment. TK activity and the crypt mitotic zone were significantly augmented in the animal group fed the stress diet. Supplementary vitamin D3 abrogated the stress diet-enhanced colonic responses to the carcinogenic insult. Colon tumor multiplicity was fourfold higher in animals fed the stress diet than in animals maintained on a standard diet. The marked rise in colonic tumor multiplicity and adenocarcinoma incidence in rats fed the stress diet was obliterated by supplemental dietary vitamin D3. Cumulatively, the present results indicate that dietary vitamin D3 impedes the neoplastic process in murine large intestine and strengthen the view that inappropriate changes in dietary components and micronutrients are contributory determinants of colorectal cancer.

Topics: 1,2-Dimethylhydrazine; Adenocarcinoma; Animals; Body Weight; Bromodeoxyuridine; Calcifediol; Calcitriol; Calcium; Calcium, Dietary; Cell Division; Cholecalciferol; Colon; Colonic Neoplasms; Disease Models, Animal; Male; Random Allocation; Rats; Thymidine Kinase

We investigated the role of 1alpha,25-dihydroxyvitamin D3 (1alpha,25(OH)2D3) in modulating tumor cell invasiveness through the extracellular matrix (ECM) and pulmonary metastasis in B16 mouse melanoma. The pretreatment of B16 cells for 48 hours with 1alpha,25(OH)2D3 significantly inhibited in vitro invasiveness through the ECM by a mechanism that is not directly correlated with the inhibition of cell proliferation. When cells were treated with 1alpha,25(OH)2D3 for only 8 hours during the assay, no inhibitory effect was observed, suggesting that pretreatment with the hormone for more than 8 hours is necessary to inhibit the invasive potential of B16 cells. The activity of B16 cells to adhere to reconstituted basement membrane (Matrigel) and type IV collagenolysis was inhibited by pretreatment of the cells with 1alpha,25(OH)2D3 for 48 hours. Cell motility was not influenced by the hormone. Mice were inoculated subcutaneously with 3 x 106 B16 cells and were given 1alpha,25(OH)2D3 (0.5 microg/kg) or vehicle daily for 28 days, beginning 1 day after tumor inoculation. In the 1alpha,25(OH)2D3-treated group, no significant inhibition in exponential tumor growth, body weight, and serum level of calcium was observed until the twenty-eighth day. The mean serum concentration of the hormone was about 50 ng/mL, and there were no significant changes in its concentration during the treatment period. In both spontaneous and experimental metastasis models of tumor-bearing mice, treatment with 1alpha,25(OH)2D3 inhibited pulmonary metastasis. These findings suggest that 1alpha,25(OH)2D3 acts on B16 cells, inhibiting invasiveness through the ECM that is caused by the inhibition of cell adhesion to the ECM and the degradation of the ECM by the cells. 1alpha,25(OH)2D3 may have the potential to inhibit metastasis by a mechanism that is not exclusively based on its anti-cell proliferative effect.

Topics: Animals; Body Weight; Calcium; Cell Adhesion; Cell Division; Cell Movement; Cholecalciferol; Collagen; DNA, Neoplasm; Extracellular Matrix; Lung Neoplasms; Melanoma, Experimental; Mice; Mice, Inbred C57BL; Neoplasm Invasiveness; Neoplasm Metastasis; Receptors, Calcitriol; Skin Neoplasms; Tumor Cells, Cultured

A target animal safety study investigated the effects of providing 25-hydroxyvitamin D3 (25-OH-D3) as a replacement for vitamin D3 in pelleted turkey feeds. Five groups of turkeys were fed diets containing vitamin D3 at 68.9 micrograms/kg feed (control) or 25-OH-D3 at concentrations of 49.5 (0.5x), 99 (1x), 495 (5x) or 990 (10x) micrograms 25-OH-D3/kg feed. The effects of 25-OH-D3 or vitamin D3 on performance, health, hematology, gross pathology and tissue concentrations of 25-OH-D3 in female and male turkeys were compared at 112 days of feeding. There was no significant difference from control in pen body weight in any of the groups. When feed conversion was calculated without taking into account body weights of birds that died during the study, there was no significant difference from control in any of the groups. When feed conversion was corrected for mortality, the only significant effect was that females at the 5x level (495 micrograms 25-OH-D3/kg feed) had improved feed conversion. Significantly increased mortality occurred during the study in the 10x (990 micrograms 25-OH-D3/kg feed) male group only. No histomorphologic tissue alterations attributable to dietary administration of 25-OH-D3 were observed in tissues examined at any dietary level of 25-OH-D3. 25-OH-D3 did not adversely affect animal health at the proposed use level of 99 micrograms/kg feed when replacing vitamin D3 in turkey rations. The proposed use level also provides at least a 5-fold margin of safety.

Topics: Animal Feed; Animal Husbandry; Animals; Body Weight; Calcifediol; Cholecalciferol; Female; Male; Turkeys

Since the vitamin D endocrine system modulates phosphorus homeostasis and regulates inorganic phosphate (Pi) uptake by the small intestine in mammals and birds, we determined the effects of dietary cholecalciferol (vitamin D3) on Pi uptake by the small intestine, Pi concentrations in the plasma, Pi concentrations in the intestinal lumen, intestinal weights, liver weights, and concentrations of vitamin D metabolites in the plasma of rainbow trout (Oncorhynchus mykiss) fed phosphorus-sufficient (0.6 g/100 g) diets. Five groups of trout initially weighing 55.8 +/- 0.6 g were fed purified diets containing 0, 300, 2,500, 10,000, and 40,000 IU vitamin D3/kg diet over a 7- to 8-day feeding period. Plasma Pi concentration was higher in trout fed 2,500-40,000 IU/kg diet (8.26 +/- 0.27 mmol/L) than in those fed 0 and 300 IU/kg (6.99 +/- 0.30). Liver weights were 30-50% greater in fish fed 0 IU/kg than in those fed 300-40,000 IU/kg. There were no significant, diet-related differences in plasma levels of 25-hydroxycholecalciferol [25(OH)D3] and 1,25 dihydroxycholecalciferol [1,25(OH)2D3]. Increasing levels of dietary cholecalciferol also did not enhance in vitro Pi uptakes by the intestine (range of means: 0.22-0.29 nmol/mg tissue. min) and Pi concentrations in the intestinal lumen (8.5-13.5 mmol/L). Pi uptake did not differ among tissues incubated in vitamin D3, 25(OH)D3, or 1,25(OH)2D3. These results demonstrate that when fish are fed P-sufficient diets, dietary cholecalciferol increases plasma Pi concentrations but decreases liver weights, alterations which are not accompanied by changes in intestinal weight, Pi uptake by the intestine, Pi concentration in the intestinal lumen, and circulating metabolites of cholecalciferol.

Topics: Animals; Body Weight; Calcifediol; Calcitriol; Cholecalciferol; Diet; Intestinal Absorption; Intestines; Liver; Oncorhynchus mykiss; Organ Size; Phosphates; Vitamin D

We previously demonstrated that a purified diet containing 3.125 microg of cholecalciferol/kg was adequate to maintain plasma concentrations of 25-hydroxyvitamin D in growing kittens. With the use of this concentration of cholecalciferol, the response of growing kittens to varying levels of calcium in purified diets was measured. Five groups (treatments 1-5), each comprised of seven weaned kittens, were given diets containing 3.8, 5.0, 6.0, 7.2 or 8. 1 g calcium/kg diet (Ca:P ratio of 1:1.25) from 9 to 18 wk of age. Two further groups of kittens (treatments 6 and 7) received similar diets containing 6.0 g Ca/kg diet, with Ca:P ratios of 1:1.55 and 1:2.61, respectively. No clinical signs of calcium deficiency were observed, i.e., growth rate, energy intake and plasma total calcium were not affected by the treatments. However, ionized calcium was significantly lower in kittens in treatment 7. Plasma phosphorus was lower in kittens in treatment 7 than in kittens in treatments 1, 2, 3 and 4, and there was a negative relationship between dietary and plasma phosphorus concentrations. Kittens in treatment 7 had a significantly higher alkaline phosphatase concentration in plasma than kittens in treatments 1, 2, 3 and 5. Kittens in treatment 1 had a lower percentage of bone minerals measured by dual-energy X-ray absorptiometry than kittens in treatments 2-6. These results indicate that the calcium requirement of growing kittens is not >6.0 g/kg diet, (calculated metabolizable energy approximately 20 kJ/g) and that kittens are not very sensitive to inverse Ca:P ratios up to 1:1.55.

Topics: Animals; Body Weight; Bone Density; Calcium; Calcium, Dietary; Cats; Cholecalciferol; Diet; Nutrition Policy; Osteocalcin; Parathyroid Hormone; Peptides; Phosphorus; Vitamin D

Adrenal medullary hyperplasia and pheochromocytomas are induced in rats by a variety of non-genotoxic agents, and we have hypothesized that these agents induce lesions indirectly by stimulating chromaffin cell proliferation. Vitamin D3, which has not been previously associated with adrenal medullary proliferative lesions, is the most potent in vivo stimulus to chromaffin cell proliferation yet identified. The present investigation utilized the vitamin D3 model to prospectively test the relationship between mitogenicity and focal proliferative lesions in the adrenal medulla and to determine early events in the pathogenesis of these lesions. Charles River Crl:CD BR rats were treated with 0; 5000; 10,000; or 20,000 IU/kg/day of vitamin D3 in corn oil (5 ml/kg) by oral intubation. Rats were killed after 4, 8, 12, or 26 weeks of treatment, following a final week of labeling with bromodeoxyuridine (BrdU) using a mini-pump. Adrenal sections were double-stained for BrdU and phenylethanolamine-N-methyl transferase (PNMT) to discriminate epinephrine (E) from norepinephrine (NE) cells or for vesicular acetylcholine transporter (VAchT) to identify cholinergic nerve endings. Vitamin D3 caused a 4-5-fold increase in BrdU labeling at week 4, diminishing to a 2-fold increase by week 26. An initial preponderance of labeled E cells gave way to a preponderance of labeled NE cells. By week 26, 17/19 (89%) animals receiving the 2 highest doses of vitamin D3 had focal adrenal medullary proliferative lesions, in contrast to an absence of lesions in control rats. The lesions encompassed a spectrum including BrdU-labeled "hot spots" not readily visible on H and E sections, hyperplastic nodules, and pheochromocytomas. Lesions were usually multicentric, bilateral, and peripheral in location, and almost all were PNMT-negative. The lesions were not cholinergically innervated, suggesting autonomous proliferation. Hot spots, hyperplastic nodules, and pheochromocytomas appear to represent a continuum rather than separate entities. Their development might involve selective responses of chromaffin cell subsets to mitogenic signals, influenced by both innervation and corticomedullary interactions. A number of non-genotoxic compounds that induce pheochromocytomas in rats are known to affect calcium homeostasis. The results of this study provide further evidence to support the hypothesis that altered calcium homeostasis is indirectly involved in the pathogenesis of pheochromocytomas, via eff

Topics: Administration, Oral; Adrenal Gland Neoplasms; Adrenal Medulla; Animals; Body Weight; Bromodeoxyuridine; Carcinogenicity Tests; Carrier Proteins; Cholecalciferol; Cholinergic Fibers; Epinephrine; Hyperplasia; Kidney; Male; Membrane Transport Proteins; Nephrocalcinosis; Norepinephrine; Organ Size; Pheochromocytoma; Rats; Rats, Sprague-Dawley; Vesicular Acetylcholine Transport Proteins; Vesicular Transport Proteins

A target animal safety study investigated the effects of providing 25-hydroxyvitamin D3 (25-OH-D3) in laying hen feed at levels ranging from 0.5 to 10 times the level commonly used for vitamin D3 supplementation in the poultry industry. Following a 28-day preconditioning period, 5 groups of laying hens were fed commercial diets containing 68.9 micrograms of vitamin D3/kg feed (control) or 41.25 (0.5x), 82.5 (1x), 412.5 (5x), or 825 (10x) micrograms of 25-OH-D3/kg feed. The study compared the effects of the control level of vitamin D3 and the various test levels of 25-OH-D3 on health, performance, hematology, and 25-OH-D3 tissue concentrations in laying hens from 0 to 112 d of treatment and on health, performance, gross pathology and histopathology from 113 to 224 d of treatment. Gross pathologic and histopathologic examination of selected tissues after 224 d revealed no lesions attributable to vitamin D toxicity at any level of test material. Concentrations of 25-OH-D3 in edible tissues at 112 d were similar for birds in the control and 1x groups. On the basis of all variables monitored, including body weight gain and feed conversion, the 10x level of 25-OH-D3 produced clear toxicity (but no mortality), the 5x level caused limited threshold toxicity, and the 1x level induced no toxicity. These results indicate that 25-OH-D3 is safe for use in laying hen feed as a source of vitamin D3 at 82.5 micrograms/kg feed (1x), with a margin of safety of approximately 5x between the proposed 1x level and the 5x level (412.5 micrograms/kg feed) that constitutes threshold toxicity in layers.

Topics: Animal Feed; Animals; Blood Cell Count; Body Weight; Calcifediol; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Eating; Female

Further studies of mimosine toxicity in broiler chicks were done to clarify a possibility of osteopathy. The mineral content and density of femur and the strength, ductility, and toughness for the index of mechanical properties significantly decreased in the 1% mimosine group, compared with those in the control and restricted groups. The stiffness had a decreasing tendency in the 1% mimosine group. Consequently, it was concluded that chicks fed ad libitum a 1% mimosine diet for 12 days developed osteopathy. The bone mineral density and the strength of the restricted group were lower than those of the control group, and those of the 1% mimosine group were still lower than those of the restricted group. Contents of pyridinoline and deoxypyridinoline in the excrement were significantly higher in the restricted group than those in the control group, but the contents in the 1% mimosine group were significantly lowest among the groups. Osteopathy in chicks fed mimosine, therefore, seemed to be done by loss of appetite and changing to a low turnover of bone caused by mimosine.

Topics: Amino Acids; Animal Feed; Animals; Body Weight; Bone Density; Calcifediol; Calcium; Chickens; Cholecalciferol; Corticosterone; Fabaceae; Femur; Iron; Magnesium; Male; Mimosine; Organ Size; Osteoporosis; Plant Poisoning; Plants, Medicinal; Zinc

Three experiments were conducted to determine the effects of high dietary levels of vitamins A and E on the utilization of cholecalciferol by broiler chicks. In Experiment 1, chicks were fed six levels of vitamin A (5,000, 10,000, 20,000, 40,000, 80,000, and 160,000 IU/kg). Cholecalciferol (vitamin D3) was not added to the basal diet but all birds were exposed to ultraviolet (UV) fluorescent light. Body weight was decreased only at levels of vitamin A of 80,000 IU/kg or above. In Experiment 2, birds were exposed to UV fluorescent light or no UV light, two levels of dietary vitamin A (1,500 and 45,000 IU/kg) and three levels of dietary vitamin D3 (0, 500, and 2,500 IU/kg) in a 2 x 2 x 3 factorial arrangement. The high level of vitamin A reduced (P < 0.001) bone ash but only at a marginal level of vitamin D3 (500 IU/kg) and when the birds were not exposed to UV light. In Experiment 3, birds were exposed to UV fluorescent light or no UV light, two levels of dietary vitamin E (10 and 10,000 IU/kg) and three levels of dietary vitamin D3 (0; 500 and 2,500 IU/ kg) in a 2 x 2 x 3 factorial arrangement. The high level of vitamin E significantly (P < 0.05) reduced body weight, bone ash, plasma calcium, and increased rickets but only at 500 IU/kg of vitamin D3. Feeding 2,500 IU/kg of vitamin D3 overcame the effects of the high level of vitamin E, causing a significant (P < 0.05) interaction. Ultraviolet light also prevented the detrimental effects of the high level of vitamin E. The results of these studies indicate that high dietary levels of vitamins A and E negatively affected the utilization of vitamin D3 only when D3 was present at a marginal level (500 IU/kg) in the diet but not when it was synthesized in the bird by exposure to UV light or supplemented at 2,500 IU/kg in the diet.

Topics: Animals; Body Weight; Calcium; Chickens; Cholecalciferol; Cohort Studies; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Incidence; Male; Phosphorus; Poultry Diseases; Rickets; Ultraviolet Rays; Vitamin A; Vitamin E

Three experiments were conducted to determine the influence of vitamin A on the utilization and amelioration of toxicity of cholecalciferol (vitamin D3), 25-hydroxycholecalciferol [25-(OH)D3], and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] in young broiler chicks. Two levels of vitamin A (1,500 and 45,000 IU/kg or 450 and 13,500 microg) were fed in all experiments. In Experiment 1, chicks were fed six levels of vitamin D3 (0, 5, 10, 20, 40, and 80 microg/kg). High dietary vitamin A decreased bone ash (P < 0.001), and increased the incidence of rickets (P < or = 0.02). Linear and quadratic responses to vitamin D3 levels were significant (P < 0.01) for body weight, bone ash, incidence and severity of rickets, and plasma calcium. In Experiment 2, six levels of 25-(OH)D3 (0, 5, 10, 20, 40, and 80 microg/kg) were added to the basal diet. Adding 25-(OH)D3 increased (P < 0.001) body weight, bone ash, and plasma calcium, and decreased rickets and plasma vitamin A. Adding 25-(OH)D3 overcame the reduction in bone ash produced by high dietary vitamin A showing a significant (P < 0.02) interaction. In Experiment 3, six levels of 1,25-(OH)2D3 (0, 2, 4, 8, 16, and 32 microg/kg) were added to the basal diet. High dietary vitamin A increased (P < 0.01) the incidence and severity of rickets. Adding 1,25-(OH)2D3 increased (P < 0.01) body weight, bone ash, plasma calcium, and reduced rickets and plasma and liver vitamin A. Adding 1,25-(OH)2D3 overcame the reduction in bone ash, and the increase in rickets produced by high vitamin A was significant (P < or = 0.05). These results indicate that high dietary vitamin A (45,000 IU/kg) interferes with the utilization of vitamin D3, 25-(OH)D3 and 1,25-(OH)2D3, increasing the requirement for each of them. Moreover, 45,000 IU/kg of dietary vitamin A ameliorated the potential toxic effects of feeding high levels of vitamin D3, 25-(OH)D3 and 1,25-(OH)2D3 to young broiler chickens. Further work is necessary to find the minimum levels of these vitamins needed to cause these effects.

Topics: Animals; Body Weight; Calcifediol; Calcitriol; Chickens; Cholecalciferol; Cohort Studies; Diet; Dietary Supplements; Dose-Response Relationship, Drug; Drug Interactions; Incidence; Male; Poultry Diseases; Rickets; Vitamin A

Four experiments were conducted to determine the effects and interactions of feeding different levels of vitamins A, cholecalciferol (vitamin D3), and E on broiler chicks. In Experiment 1, chicks were fed marginal vitamin D3 (500 IU/kg) and increasing dietary levels of vitamin A (5,000, 10,000, 20,000, 40,000, 80,000, and 160,000 IU/kg). Bone ash was reduced by 10,000 IU/kg of vitamin A in the diet and at vitamin A levels above 20,000 IU/kg of diet body weight was reduced. In Experiment 2, two levels of vitamin A (1,500 and 15,000 IU/kg) and six levels of vitamin E (10, 500, 1,000, 2,500, 5,000, and 10,000 IU/kg) were added to the basal diet. High levels of vitamins A and E significantly (P < 0.001) reduced bone ash. The vitamin A x E interaction was significant (P < or = 0.05) for rickets. In Experiment 3, the same two levels of vitamin A as Experiment 2 and six levels of vitamin D3 (500, 1,000, 1,500, 2,000, 2,500, and 3,000 IU/kg) were added to the basal diet that contained 10,000 IU/kg of vitamin E. Body weight and bone ash were increased by increasing vitamin D3 with a corresponding reduction (P < or = 0.05) in rickets. In Experiment 4, three levels of vitamin A (1,500, 15,000, and 45,000 IU/kg), three levels of vitamin D3 (500, 1,500, and 2,500 IU/kg), and three levels of vitamin E (10, 5,000, and 10,000 IU/kg) were added to the basal diet. Significant negative responses (P < or = 0.05) to increasing dietary vitamin A were observed for bone ash, rickets, and plasma and liver vitamin E. A significant (P < 0.001) increase in bone ash and plasma calcium with a corresponding reduction in rickets was observed by increasing vitamin D3. Increasing dietary vitamin E adversely affected (P < or = 0.01) bone ash, plasma calcium, and plasma and liver vitamin A concentrations. These results indicate the need for making feed with the proper ratios of vitamins A, D3, and E.

Topics: Animals; Body Weight; Calcium; Chickens; Cholecalciferol; Diet; Drug Interactions; Liver; Male; Minerals; Vitamin A; Vitamin E

Hormonal imprinting (the first encounter between the hormone and receptor after birth) is needed for the normal development of receptor. Presence of the appropriate hormone in excess, or its absence, as well as presence of hormone-like molecules able to bind to the maturing receptor in this time, can cause faulty imprinting. In this experiment the effect of neonatal treatment with a single dose of 0.05 mg cholecalciferol (vitamin D3) was studied by bone densitometry. The treatment caused significant decrease of body weight in 3-month old females and also significant reduction of bone mineral density (BMD) and bone mineral content (BMC) in males. Dexamethasone treatment of 3-month old rats for 10 days increased BMD in males and BMC in females without affecting body weight. The double treatment (vitamin D neonatally and dexamethasone when adult) decreased the body weight of both sexes and increased BMD in males, and BMC, BMD/bw and BMC/bw in both sexes, related to the control or the only vitamin D treated groups. Considering the hormonal imprinting effect of neonatal vitamin D treatment at glucocorticoid receptorial level in other experiments, similar effects also can be supposed for vitamin D itself, manifested in the changes of bone mineralization.

Topics: Animals; Animals, Newborn; Anti-Inflammatory Agents; Body Weight; Bone Density; Calcification, Physiologic; Cholecalciferol; Dexamethasone; Female; Male; Rats; Rats, Wistar; Sex Characteristics

1. Single neonatal dexamethasone (DEX) treatment significantly decreased the body weights of 5-month old male rats. There was no significant difference in females. 2. Bone mineral density (BMD) of neonatally DEX-treated male rats and bone mineral content (BMC) of double DEX-treated (neonatally and in adult age) males were reduced. 3. BMD and BMC calculated to body weight were highly significantly increased after neonatal or double DEX treatment in males. In females only BMC/body weight was elevated after double DEX treatment. 4. Adult vitamin D treatment completely compensated for the changes caused by single or double DEX treatment. 5. The results call attention to the imprinting effects of neonatal glucocorticoid treatment, which were manifested in changes of body weight and bone mineral mass. At the same time the gender-dependence of this phenomenon was demonstrated.

Topics: Aging; Animals; Animals, Newborn; Body Weight; Bone Density; Calcification, Physiologic; Cholecalciferol; Dexamethasone; Female; Glucocorticoids; Male; Rats; Rats, Wistar; Sex Factors

Cardiac function was investigated in conscious normotensive rats in which increased aortic stiffness was produced as a result of vascular calcium overload after treatment with vitamin D3 plus nicotine (VDN rats, n = 16; controls, n = 17). Baseline stroke volume, cardiac output, and cardiac response to a venous volume overload were unchanged after 1 mo of exposure to increased aortic stiffness, as were baseline venous return and total vascular capacitance. The latter was estimated from the change in mean circulatory filling pressure after modification of circulatory volume. Cardiovascular reflexes were modified in VDN rats. Bradycardia evoked by an increase in arterial PCO2 (PaCO2) or hypotensive hemorrhage was more pronounced. The PaCO2-induced bradycardia was accompanied by a fall in cardiac output in VDN rats but not in controls. In VDN rats, the attenuation of sympathetic reflexes may explain the slower recovery of blood pressure after hypotensive hemorrhage. In conclusion, a chronic increase in aortic stiffness does not compromise cardiac performance, but cardiovascular reflexes are impaired in VDN rats. Whether this is because of the increase in aortic stiffness or the effect of VDN treatment on the baroreceptors or other components of the reflex arc remains to be elucidated.

Topics: Animals; Aorta; Blood Volume; Body Weight; Calcium; Carbon Dioxide; Cardiac Output; Cholecalciferol; Elasticity; Heart Ventricles; Hemodynamics; Hemorrhage; Nicotine; Rats; Rats, Wistar

The effects of the excessive administration of the vitamin AD3E(V-AD3E) premix, vitamin A (V-A) or vitamin D3 (V-D3) on experimental development of Hyena disease in the calves were examined. Hyena disease was recognized in 4 calves, both of the 2 calves administered a high dose of V-AD3E premix (V-A 3,000,000, V-D3 300,000, and V-E 1,200 IU/day, V-AD3E group), 1 of the 2 calves administered a half dose of the V-AD3E premix, and 1 of the 2 calves administered only V-A (V-A 3,000,000 IU/day, V-A group) when each vitamin was administered orally for 10 days from 1 week after birth. Both of 2 calves administered only V-D3 (V-D3 300,000 IU/day) did not developed. In the 4 calves with Hyena disease (Hyena calves), the plasma retinylpalmitate showed high values which was suggesting the hypervitaminosis A, and the epiphysial growth plate was narrow and destroyed structure of column. Compared with the Hyena calf in the V-A group, the Hyena calves in the V-AD3E group showed earlier appearance time of Hyena disease, lower growth rate and shorter lengths of fore and hind limb bones. In conclusion, the present findings suggested that excessive V-A administration to suckling calves might cause Hyena disease by V-A effects to the epiphysial growth plate, moreover such effects may be promoted by the V-D3.

Topics: Aging; Animals; Body Height; Body Weight; Bone Diseases; Cattle; Cattle Diseases; Cholecalciferol; Food, Fortified; Growth Plate; Male; Radiography; Vitamin A

Chronic consumption by rats of diets rich in sugars or sugar alcohols leads to an increased incidence of pheochromocytomas. This relationship is hypothesized to be based on altered Ca2+ homeostasis due to increased intestinal Ca2+ absorption. Other agents associated with pheochromocytomas in rats in long-term toxicity studies have been shown to increase chromaffin cell proliferation, leading to the suggestion that the tumors occur secondarily to increased chromaffin cell turnover. We have demonstrated marked stimulation of chromaffin cell proliferation by vitamin D3, a potent stimulus to Ca2+ absorption not previously associated with adrenal medullary toxicity. This effect is detectable during the first week of dietary supplementation and persists throughout a 4-week time course. Lactose and xylitol, representative of sugars and sugar alcohols associated with pheochromocytomas, are also mitogenic but to a lesser extent, with their effects first detectable during Week 4 of dietary supplementation. Vitamin D3, its active metabolite calcitriol, lactose, and xylitol all fail to stimulate proliferation of rat chromaffin cells in vitro. The mitogenic effects of these agents may be mediated presynaptically in vivo. The data suggest that altered Ca2+ homeostasis may increase chromaffin cell proliferation and support the hypothesis that diets containing high concentrations of sugars and sugar alcohols cause pheochromocytomas in rats secondarily by this mechanism.

Topics: Adrenal Medulla; Animals; Body Weight; Calcium; Cell Division; Cholecalciferol; Chromaffin Cells; Diet; Kidney; Lactose; Male; Organ Size; Rats; Xylitol

We conducted two safety studies of 25-hydroxycholecalciferol [25(OH)D3] in poultry broilers at levels ranging from 1 to 200 times those commonly used for cholecalciferol (vitamin D3) supplementation in the industry. In the first experiment, 1-d-old male and female broiler chickens were fed commercial diets containing either vitamin D3 or 25(OH)D3 at concentrations of 69, 207, and 690 micrograms of 25(OH)D3/kg of feed. The second experiment compared effects of 25(OH)D3 and vitamin D3 on performance and survival of broilers at levels ranging from 1 to 200 times the basal level of 69 micrograms/kg feed. When 25(OH)D3 was fed in equal amounts (wt/wt) to vitamin D3, there was an increase in body weight and a decrease (improvement) in adjusted feed efficiency in both experiments, but the changes were significant only in the first experiment. In the first experiment, serum 25(OH)D3 concentrations increased from 13.3 +/- 4.3 to 42.5 +/- 18 ng/mL in birds fed vitamin D3 or 25(OH)D3, respectively, and rose to 246 +/- 38 ng/mL in birds fed the highest level of 25(OH)D3. Tissue 25(OH)D3 concentrations were much lower than serum concentrations and were highly correlated to the latter, regardless of dietary treatment. In Experiment 2, there was some evidence of renal calcification in birds fed 25(OH)D3 at 10 times the basal level, whereas dietary levels of vitamin D3 of 50 times the basal level were required to show some evidence of renal calcification. On the basis of both renal calcification and body weight, the present studies would suggest that 25(OH)D3 is 5 to 10 times more toxic than vitamin D3.

Topics: Animals; Body Weight; Calcifediol; Chickens; Cholecalciferol; Consumer Product Safety; Female; Food, Fortified; Male; Mortality; Nephrocalcinosis; Tissue Distribution

Effect of vitamin D3 administration (12,000 IU/100 g body wt.) on levels of serum calcium and inorganic phosphorus levels in the smooth water snake, Enhydris enhydris was investigated. Hypercalcemia and hyperphosphatemia was observed from day one till the end of the experiment (day 14). Maximum values were recorded on the 4th day followed by a steady decline.

Topics: Animals; Body Weight; Calcium; Cholecalciferol; Female; Injections, Intraperitoneal; Male; Phosphorus; Snakes

The effects of 1 alpha-vitamin D3 were studied for 6 months in 2-month-old male and female rats on a moderately low calcium diet with or without low-dose prednisolone treatment. Both cortical bone mechanical and biochemical properties were examined. Femoral bone specimens were subjected to torsional loading tests. With age, bone strength and stiffness increased in both sexes, accompanied by an increased degree of mineralization (bone ash and calcium concentrations). During growth, strength and stiffness increased more in male than in female rats. When 1 alpha-vitamin D3 (0.5 micrograms/kg/day) was given alone, bone mechanical competence improved significantly whereas insulin-like growth factor-I (IGF-I) and calcium concentrations in the bone matrix were significantly reduced. Treatment with low-dose prednisolone (0.5 mg/kg/day) alone did not influence bone mechanical properties compared with intact control rats (without prednisolone) although a significant reduction in calcium concentration and an increased phosphorus concentration were measured. A combined therapy with prednisolone and 1 alpha-vitamin D3 significantly increased bone strength, toughness, and stiffness compared with control bones. Both mineralization degree (ash and calcium concentration) and IGF-I concentration were decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Biomechanical Phenomena; Body Weight; Bone Density; Bone Matrix; Calcification, Physiologic; Calcium; Calcium, Dietary; Cholecalciferol; Drug Synergism; Female; Femur; Insulin-Like Growth Factor I; Male; Osteocalcin; Phosphorus; Prednisolone; Random Allocation; Rats; Rats, Sprague-Dawley; Sex Characteristics; Transforming Growth Factor beta; Weight-Bearing

Sertoli cells from immature (18-20 day old) Siberian hamsters (Phodopus sungorus) raised in a long photoperiod (LD; 16hL:8hD) or a short photoperiod (SD; 6hL:18hD) were cultured and exposed to follicle-stimulating hormone (FSH) and/or vitamin D3 (D3) in vitro. D3 did not stimulate lactate production when added alone, but significantly augmented the stimulatory action of FSH on lactate production by Sertoli cells from both LD- and SD-exposed hamsters. Hamsters raised in LD or SD were injected daily with D3 for 10 days starting at 18 days of age. This treatment resulted in a significant increase in the testicular weight of hamsters raised in LD in which circulating FSH levels are high. In contrast, testicular weight was not altered by D3 treatment in SD hamsters in which circulating levels of FSH are low. We conclude that D3, probably after hydroxylation to 1,25(OH)2 vitamin D3, modulates the action of FSH on testicular growth and Sertoli cell function.

Topics: Animals; Body Weight; Cells, Cultured; Cholecalciferol; Cricetinae; Drug Synergism; Follicle Stimulating Hormone; Lactates; Lactic Acid; Male; Organ Size; Phodopus; Photoperiod; Sertoli Cells; Testis

The interaction between 17 beta-estradiol (E2), vitamin D3 (D3), and dietary Ca on the activities of Ca-ATPase and alkaline phosphatase (AP) was determined in the intestine of young female chicks. Chicks (n = 36) were assigned to two groups, one of which was transferred to a low Ca (0.2%) diet and the other maintained on a regular diet. One week later, each group was further divided into three subgroups and given daily injections of 0(oil), 0.25, or 0.5 mg E2/kg body wt for 14 days. E2 treatment as well as low dietary Ca significantly increased AP activity (P < 0.05), whereas the highest E2 dose decreased jejunal Ca-ATPase (P < 0.05). In a separate study, day-old chicks (n = 40) fed a purified diet supplemented with or without D3 for 24 days were divided into two subgroups and administered daily injections of either 0 or 0.25 mg estrogen 3-benzoate/kg body wt for 5 days. E2 alone or in combination with D3 failed to change Ca-ATPase activity in either the duodenum or the jejunum. However, E2 enhanced the D3-stimulated AP activity measured in the supernatant of duodenum (D3, P < 0.001; E2, P > 0.05; E2 x D3, P < 0.05) and jejunum (D3, P < 0.001; E2, P > 0.05; E2 x D3, P = 0.06). Daily injections of 0.5 mg E2/kg body wt for 6 days to 6-week-old D3-adequate chicks (n = 16) significantly increased AP activity in jejunum but not in liver and kidney (P < 0.05). In conclusion, E2 treatment enhanced the activity of intestinal AP but not Ca-ATPase. This enhancement was independent of dietary Ca, but was D3-dependent and tissue specific. The results suggest that the pubertal increase in plasma E2 can affect Ca absorption from the intestine by increasing the activity of AP.

Topics: Aging; Alkaline Phosphatase; Animals; Body Weight; Calcium-Transporting ATPases; Calcium, Dietary; Chickens; Cholecalciferol; Diet; Dose-Response Relationship, Drug; Drug Interactions; Estradiol; Female; Injections, Subcutaneous; Intestines

The purpose of this study was to investigate whether vitamin D3 deficiency affects the cardiac function of chick hearts directly or whether the influence is secondary through the hormone's effect on serum calcium levels. To this end, three experimental groups were studied: (a) the control group of vitamin D3 supplemented chicks, Ds, (b) vitamin D3 deficient chicks, Dd, and (c) vitamin D3 supplemented hypocalcemic chicks raised on decreased calcium levels, Dh. The three groups were compared by checking hemodynamic, metabolic and membrane parameters. Total and ionized serum calcium concentrations in the Dh and Dd groups were found to be lower than in the Ds group. Perfusion of the isolated hearts with solutions containing various calcium concentrations (1, 1.5 and 2.5 mM) induced enhanced contractility levels, the magnitude of which was dependent on the difference between the in vivo and perfusate calcium levels. Thus, the inotropic effect was similar and more enhanced for the two hypocalcemic groups. The differences in hemodynamic behaviour could not be explained by variations in the levels of the high energy compounds and acidity, since similar ATP, creatine phosphate and intracellular pH levels were detected for both Ds and Dd groups. However, membrane studies revealed an increase in the number of slow calcium channels for the two hypocalcemic groups and this may be the possible mechanism for the differences in the contractile activity. In conclusion, our study strongly suggests that the effects of vitamin D3 on the heart is mediated only indirectly through its effect on serum calcium levels.

Topics: Animals; Body Weight; Calcium; Chickens; Cholecalciferol; Heart; Magnetic Resonance Spectroscopy; Myocardial Contraction; Myocardium; Nitrendipine; Organ Size; Vitamin D Deficiency

Treatment of young rats with vitamin D3 and nicotine produced a 35-fold increase in the calcium content of the aorta and a 4-fold increase in the calcium content of the mesenteric arterial bed. Blood pressure was not modified. In vitro, aortic rings and mesenteric arterial bed preparations from such animals showed diminished vasoconstrictor responses to norepinephrine. After precontraction with norepinephrine, the endothelium-dependent vasodilator, carbachol, produced vasorelaxation. This latter effect was attenuated in aortic rings and mesenteric arterial bed preparations from animals previously treated with vitamin D3 and nicotine, but the vasodilator effect of sodium nitroprusside (which is independent of the endothelium) was unchanged. Prolonged treatment with the calcium entry blocker, isradipine, at a dose (1 mg/kg, i.p.) which had no effect on blood pressure, prevented calcium overload of the mesenteric arterial bed, but did not modify aortic calcium overload. Isradipine treatment had no effect on vasoconstrictor responses to norepinephrine in vitro. Such treatment did, however, restore the endothelium-dependent vasodilator effect of carbachol in the mesenteric arterial bed (but not in aortic rings). In conclusion, in a rat model of vascular calcium overload produced by administration of vitamin D3 plus nicotine, chronic treatment with a low dose of the calcium entry blocker, isradipine, restored the endothelium-dependent vasorelaxant effect of carbachol in the mesenteric arterial bed, but not in the aorta.

Topics: Animals; Aorta, Thoracic; Blood Pressure; Body Weight; Calcium; Calcium Channel Blockers; Cholecalciferol; Dihydropyridines; Endothelium, Vascular; Heart Rate; Isradipine; Male; Mesenteric Arteries; Models, Biological; Muscle Relaxation; Muscle, Smooth, Vascular; Nicotine; Rats; Rats, Inbred Strains; Time Factors

Pamidronate (disodium 3-amino-1-hydroxypropylidene-1,1-bisphosphonate pentahydrate, CGP 23339A, CAS 57248-88-1) has been show to provide a potent antihypercalcemic effect through the inhibition of calcium release from the bone. The time course study on the antihypercalcemic effect of pamidronate was performed using a rat hypercalcemia model induced by orally administered cholecalciferol. The onset of the antihypercalcemic effect was observed within 48 h after a single i.v. injection of pamidronate at 1 mg/kg and this effect was sustained for 19 days. The time course of the antihypercalcemic effect of pamidronate in combination with calcitonin was also examined in the same model. The onset of the antihypercalcemic effect was observed within 4 h after combination therapy with a single i.v. injection of pamidronate at 1 mg/kg and successive i.m. injections of calcitonin at 3.2 IU/kg and the effect was of sufficient duration. These results suggest that pamidronate has a pronounced effect in controlling hypercalcemia and provides a long-lasting effect by a single i.v. administration. Moreover, the use of pamidronate in combination with calcitonin may be useful when a quicker onset of action is required clinically.

Topics: Animals; Body Weight; Calcitonin; Calcium; Cholecalciferol; Diphosphonates; Female; Hypercalcemia; Pamidronate; Phosphates; Rats; Rats, Inbred Strains

1. The haemodynamic effects of S-12968-(-), a new dihydropyridine calcium entry blocker (enantiomer of S-11568), were compared with those of the stereoisomer, S-12967-(+), nifedipine, and sodium nitroprusside. 2. A first experiment was performed in conscious, young male rats chronically implanted with femoral artery and vein cannula and repeated in rats previously treated with vitamin D3 and nicotine. Such treatment produces marked vascular calcium overload, especially of the compliance arteries, with no overt sign of toxicity as far as can be judged from the plasma profile. 3. In conscious rats the hypotensive effects of S-12968-(-), nifedipine and sodium nitroprusside were of similar potency. The falls in blood pressure produced by nifedipine and sodium nitroprusside were accompanied by reflex tachycardia which was less marked in the vascular calcium overload model. S-12968-(-) did not induce reflex tachycardia. S-12967-(+) increased blood pressure in both models. 4. A second experiment was performed in open-chest pentobarbitone-anaesthetized rats with electromagnetic flowprobes on the ascending aorta. In controls the falls in blood pressure produced by low doses (0.1 and 0.3 mg kg-1, i.v.) of S-12968-(-) were accompanied by falls in total peripheral resistance. The higher dose (1 mg kg-1, i.v.) of S-12968-(-) produced no change in total peripheral resistance, and in rats pretreated with vitamin D3 and nicotine, cardiac output fell. 5. In conclusion, S-12968-(-) appears to have a dual action and to lower blood pressure at higher doses at least in part by a cardiac effect. This phenomenon is more pronounced in rats pretreated with vitamin D3 and nicotine.6. S-12967-(+) resembles a calcium channel activator in this model.

Topics: Animals; Blood Pressure; Body Weight; Calcium; Calcium Channel Blockers; Cardiac Output; Cholecalciferol; Dihydropyridines; Heart Rate; Hemodynamics; Magnesium; Male; Nicotine; Nifedipine; Nitroprusside; Rats; Stereoisomerism; Vascular Resistance

The effects of ursodeoxycholic acid (UDCA) and 1 alpha-hydroxyvitamin D3 on pathophysiological changes following massive resection of the distal small bowel (75%) were investigated by using adult beagle dogs. After surgery, body weight decreased, watery diarrhea occurred, and the transit time of the alimentary tract shortened. These undesirable consequences lessened markedly after oral administration of UDCA, though 1 alpha-hydroxyvitamin D3 was not effective. Plasma levels of both 25-hydroxyvitamin D3 and 24, 25-dihydroxyvitamin D3 decreased after surgery, while plasma 1 alpha, 25-dihydroxyvitamin D3 concentrations remained unchanged during the observation period of six months. Although fasting plasma concentrations of total bile acid were not reduced, the integrated response to a meal decreased significantly after surgery in spite of the administration of UDCA. The concentration of UDCA in the gallbladder bile increased markedly in dogs which received UDCA. Taurine-conjugated bile acids accounted for more than 90% of the gallbladder bile. Postprandial hypergastrinemia occurred following the massive small bowel resection in the control group and in the group which received 1 alpha-hydroxyvitamin D3 alone, while it did not occur in the group given UDCA together with 1 alpha-hydroxyvitamin D3. These results indicate that administration of UDCA after massive resection of the small intestine is effective in maintaining good nutritional state.

Topics: Administration, Oral; Animals; Bile; Bile Acids and Salts; Body Weight; Cholecalciferol; Dogs; Female; Food; Gastrins; Intestine, Small; Ursodeoxycholic Acid

Treatment of young rats with vitamin D3 plus nicotine, which has been proposed as a model of cardiovascular calcium overload, produced an increase in the calcium content of the mesenteric arterial bed and lowered in vitro vasoconstrictor responses to norepinephrine and serotonin. Attenuation of the vasoconstriction induced by norepinephrine by the endothelium-dependent vasodilators, carbachol and histamine, was diminished, but the effects of sodium nitroprusside and papaverine were unchanged. The vitamin D3 plus nicotine model may be useful for the study of the involvement of calcium overload in vascular endothelial dysfunction.

Topics: Animals; Body Weight; Calcium; Carbachol; Cholecalciferol; Endothelium; Histamine; Male; Muscle Relaxation; Muscle, Smooth, Vascular; Nicotine; Nitroprusside; Norepinephrine; Papaverine; Rats; Rats, Inbred Strains; Serotonin

Tibiae were removed from 300 75-wk-old laying hens for tibia strength analysis using two methods, direct photon absorptiometry and tibia breaking strength. Left tibiae with flesh intact were used for bone density determination with direct photon absorptiometry. Right tibiae were cleaned and dried for determination of tibia weight and tibia breaking strength. Partial correlation coefficients were estimated among bone density, tibia breaking strength, tibia weight, and body weight. A significant correlation was observed between tibia breaking strength and bone density measurements (r = .66, P less than or equal to .0001). Tibia weight and tibia breaking strength were also significantly correlated (r = .62, P less than or equal to .0001), as well as bone weight and bone density (r = .71, P less than or equal to .0001). Tibia weight and BW were also significantly correlated (r = .66, P less than or equal to .0001), necessitating covariance adjustment for BW. Bone densitometry measurements are less variable than tibia breaking strength measurements, and bone densitometry does not require cleaning bones of flesh before measurement.

Topics: Absorptiometry, Photon; Animals; Body Weight; Bone Density; Chickens; Cholecalciferol; Densitometry; Female; Multivariate Analysis; Tibia

A study was conducted to test the hypothesis that growing dogs do not require supplementation with cholecalciferol (vitamin D-3) in a nonpurified extruded diet. Twenty-eight weanling pups from four litters of English pointers and two litters of German Shepherd dogs were allotted equally to two groups by gender and weight. Dogs were raised in indoor-outdoor kennel runs for the 102-wk evaluation. One group was fed a diet that contained no added vitamin D while the other group was fed the same diet to which had been added 60.5 micrograms cholecalciferol/kg diet. Both diets contained approximately 14% calcium and 1.0% phosphorus. Growth as measured by body weight and length, serum calcium, phosphorus and alkaline phosphatase and urine hydroxyproline were not significantly different (P greater than 0.05) between the two treatment groups. There was no relationship between dietary treatment and nutritional secondary hyperparathyroidism (NSH), rickets or other skeletal abnormalities. The data support the concept that addition of vitamin D to typical commercial dog foods for purposes of prevention or amelioration of rickets, NSH or other skeletal diseases is unnecessary.

Topics: Alkaline Phosphatase; Animal Feed; Animals; Body Weight; Breeding; Calcium; Cholecalciferol; Dog Diseases; Dogs; Femur; Hip Joint; Housing, Animal; Hydroxyproline; Pelvis; Phosphorus; Radiography; Rickets; Weaning

Male broiler chicks (1-d-old; Ross one) were given either a control diet containing recommended levels of phosphorus, calcium and cholecalciferol or experimental diets low in P and with variable levels of Ca (normal and low) and cholecalciferol (normal or high). The low-P diet with normal levels of Ca and cholecalciferol induced a hypophosphataemia and a hypercalcaemia which was reflected in reduced tibia length and weight and in reduced Ca, P and magnesium contents of tibia. The phytate digestibility remained normal while the retention of P and Ca fell significantly. The lowering of Ca alone elevated phytate digestibility and restored P and Ca retention. The hypercalcaemia and hypophosphataemia remained and tibia mineralization remained impaired. The raising of cholecalciferol alone dramatically increased phytate digestibility and the retention of Ca and P. While this remedied the hypercalcaemia, the hypophosphataemia persisted as did the diminution of tibia weight. The simultaneous lowering of dietary Ca and elevation of cholecalciferol on low-P diets restored all variables to the levels for the control diet. Circulating levels of 1,25-dihydroxycholecalciferol were significantly elevated by low-P diets, more so with high cholecalciferol intakes. However, Ca did not influence 1,25-dihydroxycholecalciferol levels in plasma.

Topics: Animals; Body Weight; Calcification, Physiologic; Calcitriol; Calcium, Dietary; Chickens; Cholecalciferol; Digestion; Male; Phosphorus, Dietary; Phytic Acid; Tibia

In lactating rats consuming a commercial diet adequate in calcium, phosphorus and vitamin D, the effect of supplementation of 3000 IU and 7,500 IU of vitamin D3 on the lactational performance of the dams and soft tissue and skeletal growth in the pups has been investigated. On 28th day of age, the pups in the supplemented groups were significantly heavier than in the control group. Study of the indices of cellular growth in the liver and gastrocnemius muscle revealed that the increase in the soft tissue weight was due to a significant increase in protein, RNA and DNA contents (cellular hyperplasia) without any change in protein/DNA ratio (cell size). In the tibia, compared to controls, the dry bone weight and ash weight were more in the supplemented groups, but ash weight/dry bone weight ratio was not altered. The improvement in the neonatal growth was most probably due to the greater milk yield observed in the dams in supplemented groups and not due to any anabolic effect in the pups since direct administration of 500 IU or 1,000 IU of vitamin D3 in 10 day old pups did not increase their body weight.

Topics: Animals; Animals, Newborn; Animals, Suckling; Body Weight; Cholecalciferol; Dose-Response Relationship, Drug; Eating; Female; Lactation; Milk; Pregnancy; Rats; Rats, Inbred Strains

1. Treatment of young rats with vitamin D3 plus nicotine produced 31 and 4 fold increases in the calcium content of the aorta and the mesenteric arterial bed, respectively. 2. Aortic rings and perfused mesenteric arterial beds from vitamin D3/nicotine-treated animals showed a diminished contractile response to noradrenaline in vitro. 3. In vascular preparations from vitamin D3/nicotine-treated animals, precontracted with noradrenaline, relaxation by the endothelium-dependent vasodilator, carbachol, was attenuated but responses to sodium nitroprusside were not modified. 4. Prolonged treatment with the angiotensin I converting enzyme inhibitor, perindopril, at a dose (1 mg kg-1) which did not significantly modify blood pressure, failed to prevent vascular calcium overload. 5. Perindopril treatment diminished noradrenaline-evoked vasoconstrictor responses of aortic rings in both groups, but restored responses in mesenteric arterial beds of vitamin D3/nicotine-treated rats. 6. Perindopril treatment also restored the maximal responses to carbachol of both aortic rings and mesenteric arterial beds of vitamin D3/nicotine-treated rats. 7. In conclusion, in the vitamin D3 plus nicotine model of calcium overload, reduced endothelial-mediated relaxation can be prevented by perindopril treatment.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Aorta, Thoracic; Blood Pressure; Body Weight; Calcium; Carbachol; Cholecalciferol; Endothelium, Vascular; Heart Rate; In Vitro Techniques; Indoles; Magnesium; Male; Muscle Relaxation; Muscle, Smooth, Vascular; Nicotine; Nitroprusside; Norepinephrine; Perindopril; Rats; Rats, Inbred Strains; Splanchnic Circulation

Experiments were conducted to investigate the effect of feeding cimetidine (CIMET), ranging from 0 to 750 mg/kg, on vitamin D3 metabolism and eggshell calcification in laying hens fed two levels of vitamin D3 (500 and 2,000 ICU/kg). Final BW and feed intake were not significantly affected by either CIMET or vitamin D3 level. Feeding 500 and 750 mg of CIMET significantly decreased total egg production in hens fed either level of vitamin D3, but no differences were observed at lower CIMET levels. Tibia ash decreased significantly in hens fed 150 to 750 mg of CIMET, regardless of the vitamin D3 level. Plasma Ca and inorganic P concentrations were decreased in hens fed high CIMET levels (500 and 750 mg/kg) at Week 2, but no differences were observed at Week 4. Feeding CIMET (500 and 750 mg/kg) significantly decreased plasma 25-hydroxycholecalciferol (25-OHD3) levels at Week 2 in hens fed both vitamin D3 diets but not at Week 4. Eggshell breaking force, shell thickness, and percentage shell weight were decreased significantly by CIMET in all experiments; however, in one experiment, shell quality recovered by Week 8. These results suggest that the CIMET-induced reduction in bone mineralization, eggshell quality, and plasma 25-OHD3 levels could be due to interference of CIMET with vitamin D3 metabolism in vitamin D3-replete laying hens. Shell quality decreased in CIMET-treated hens fed the higher vitamin D diet even though 250-HD3 plasma levels were three times higher than in hens fed the lower vitamin D diet, suggesting that CIMET affected shell quality through some mechanism other than inhibition of 250-HD3 synthesis.

Topics: Animal Feed; Animals; Body Weight; Calcifediol; Calcium; Chickens; Cholecalciferol; Cimetidine; Eating; Egg Shell; Female; Oviposition

We have previously shown that depletion of vitamin D3 in rats results in a large increase in the contractile function of isolated hearts (R. E. Weishaar, J. Clin. Invest. 79: 1706-1712, 1987). To characterize the mechanism responsible for this increase, the effect of vitamin D3 depletion on key physical and morphological properties of cardiac muscle was examined. Depletion of vitamin D3 increased the heart weight/body weight ratio. This increase could neither be blocked by limiting hypocalcemia nor reversed by restoring increasing serum calcium levels. The cardiomegaly observed 9 wk after vitamin D3 depletion was not accompanied by an increase in myocardial water content or leakage of myocardial creatine phosphokinase and was not caused by myocardial cell hypertrophy. Histological examination of ventricular muscle from vitamin D3-deficient rats revealed a significant decrease in myofibrillar area and a significant increase in extracellular space. The increase in extracellular space was accompanied by a significant increase in myocardial collagen. Prevention of hypocalcemia in the vitamin D3-deficient rats did not prevent the increase in myocardial collagen. Such alterations in the physical and morphological properties of myocardial tissue might represent the basis for the change in myocardial contractile function that accompanies lengthy periods of vitamin D3 deficiency.

Topics: Animals; Body Weight; Calcium; Catecholamines; Cholecalciferol; Creatine Kinase; Extracellular Space; Heart; Hormones; Magnesium; Male; Microscopy, Electron; Myocardial Contraction; Myocardium; Organ Size; Rats; Rats, Inbred Strains; Vitamin D Deficiency

This study was designed to investigate, in some detail, the relative effects of the hormonal form of vitamin D (1,25-dihydroxycholecalciferol) on duodenal Pb and Ca absorption as a function of dietary Pb level. When cholecalciferol-deficient chicks were chronically repleted with physiologic levels of 1,25-dihydroxycholecalciferol (1,25(OH)2D3), as the sole source of the vitamin, 203Pb and 47Ca absorption were enhanced over 4- and 8-fold, respectively. Ingestion of Pb during the repletion period had no significant effect on the intestinal Ca absorption response to 1,25-(OH)2D3 even at a very high dietary Pb level. The efficiency of intestinal 203Pb absorption was, however, significantly diminished by dietary Pb, in an apparent dose-dependent fashion. The results indicate that the extent to which systemic Ca homeostatic mechanisms influence intestinal Pb absorption is dependent, in large part, on Pb status.

Topics: Alkaline Phosphatase; Animals; Body Weight; Calbindins; Calcitriol; Calcium; Chickens; Cholecalciferol; Diet; Dose-Response Relationship, Drug; Duodenum; Intestinal Absorption; Lead; Male; Phosphorus; S100 Calcium Binding Protein G; Vitamin D Deficiency

This study was conducted to determine the effect of feeding vitamin D3(D3) metabolites on BW of hen, weight of uterus, plasma Ca, jejunal and uterine adenosine triphosphatase (ATPase), and carbonic anhydrase. At 416 days of age each of 7 groups of laying hens was fed the basal ration supplemented with one of 7 concentrations (micrograms per kg) of D3 or its metabolites as treatments: 0 micrograms of D3; 27.5 micrograms of D3; 3, 5, or 7 micrograms of 1,25(OH)2D3; 5 micrograms of 24,25(OH)2D3; and 5 micrograms of 24,25(OH)2D3 plus 5 micrograms of 1,25(OH)2D3. Treatment effects were compared at various periods after the start of the study. Hens fed the unsupplemented ration had lower (P less than .05) values for all traits than hens fed the D3-supplemented ration by 162 days after the start of treatment. In a comparison of all dietary treatments except the one involving 0 micrograms D3, from 154 to 161 days after the start of the experiment, treatment effects were significant (P less than or equal to .05) for BW, uterine ATPase, and carbonic anhydrase; hens fed 5 micrograms of 24,25(OH)2D3 per kg of ration ranked the lowest of all treatment groups for these traits. Hens fed 27.5 micrograms of D3 and those fed 5 micrograms of 1,25(OH)2D3 per kg of ration did not differ (P greater than .05) for any traits studied. The results suggest that 5 micrograms of 1,25(OH)2D3 per kg of ration can replace 27.5 micrograms of D3 per kg of ration but that 5 micrograms of 24,25(OH)2D3 per kg of ration tends to have a negative effect on physiological systems of the hen.

Topics: 24,25-Dihydroxyvitamin D 3; Adenosine Triphosphatases; Animals; Body Weight; Calcitriol; Calcium; Carbonic Anhydrases; Chickens; Cholecalciferol; Female; Jejunum; Organ Size; Random Allocation; Uterus

Four experiments were conducted to determine the effect of dietary cholecalciferol (vitamin D3), 25-hydroxycholecalciferol (25-OHD3) and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on the changes in growth, feed efficiency and bone ash, and the incidence, severity and number of #3 scores of tibial dyschondroplasia caused by the addition of disulfiram to the diet. The basal diet used was low in calcium and high in phosphorus and chlorine and known to promote a high incidence of tibial dyschondroplasia in broiler chickens. The chickens in all experiments received enough ultraviolet radiation from fluorescent lights in the pens to nearly satisfy their need for vitamin D. The addition of disulfiram to the diet caused an increase in most of the measurements indicating development of tibial dyschondroplasia in all of the experiments, and caused a decrease in bone ash in two of the experiments and a decrease in growth and gain:feed in one experiment. The addition of D3 to a diet containing no D3 caused higher bone ash and lower incidence of tibial dyschondroplasia in the absence or presence of disulfiram. The effects of the addition of 25-OHD3 to diets containing approximately five times the requirement of D3 in the absence and presence of disulfiram caused variable results. The addition of 1,25-(OH)2D3 to the D3-supplemented diet in the absence or presence of disulfiram caused dramatic increases in bone ash and a decrease in most of the criteria used to measure development of tibial dyschondroplasia. There was no indication of interaction of the effects of D3, 25-OHD3 and 1,25-(OH)2D3 with the action of disulfiram.

Topics: Animals; Body Weight; Bone and Bones; Calcifediol; Calcitriol; Calcium; Chickens; Cholecalciferol; Diet; Disulfiram; Male; Minerals; Osteochondrodysplasias; Poultry Diseases; Tibia

Variable quantities of vitamin D3 (D3) ranging from 0 to 20,000 IU D3/kg of diet were incorporated in a corn-soybean meal basal diet and fed to male broiler chicks from day-old until 56 days of age. Four experiments were conducted to determine: 1) the requirement of D3 for growth and bone calcification of normal chicks, 2) the requirement of D3 for deficient chicks, and 3) if feeding up to 20,000 IU D3/kg of diet affects bone metabolism or increases the incidence of leg abnormalities. The parameters measured included: body weight, feed consumption, feed conversion, mortality rate, ionic and total serum calcium, kidney calcium, total blood phosphorus, tibial ash, tibial breaking strength, and tibial length. In addition, the type and the incidence of occurrence of skeletal abnormalities were recorded. The data indicate that feeding less than 200 IU D3/kg of diet produced significantly lower body weights, feed consumption and conversion values, serum ionic calcium, total serum calcium, tibial breaking strength, and percentage tibial ash values (P less than .05). For example, rachitic chicks fed 200 IU D3/kg of diet had significantly lower (P less than .05) levels of ionic calcium at 21 days than rachitic chicks fed 300, 400, or 1,500 IU D3/kg of diet. The optimal level of D3 for 0 to 56-day-old male broiler chicks, based on body weight and percentage tibial ash, is 400 IU D3/kg of diet. The vitamin D3 requirement for deficient chicks repleted with D3 appears to be between 300 to 400 IU D3/kg of diet. Feeding 1,500 to 20,000 IU D3/kg of diet does not appear to alter bone metabolism or increase the incidence of leg abnormalities.

Topics: Abnormalities, Drug-Induced; Animals; Body Weight; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Female; Male

Twenty-four male goats, approximately 2 to 4 wk of age, were allotted to four dietary treatments in a 2 X 2 factorial design and were fed a basal milk diet at 12.5% body weight for 20 wk. Vitamin D3 was added to the milk in two different amounts with and without supplemental CaCO3. At the end of wk 7, corn was added to all diets at 1% body weight. Over 20 wk, average daily gain was unaltered by addition of Ca or vitamin D3 to the diet. When corn was added to the diet, gains increased from 48 to 180 g/d. Plasma Ca concentrations were not affected by dietary treatment. Supplemental Ca decreased plasma Mg concentrations. Corn supplementation curtailed a depression in plasma Mg and seemed to prevent a whole milk-induced hypomagnesemia. Fecal excretion of all minerals measured was increased in goats fed supplemental Ca. Dietary Ca increased urinary Ca but decreased urinary Mg. Percentage of apparent absorption of Ca, Mg, and total ash was lower in Ca-supplemented goats, as was apparent retention of Ca and Mg. The physiological responses reported suggest the goat as a potential research model for mineral metabolism studies in other ruminants.

Topics: Animals; Body Weight; Calcium, Dietary; Cholecalciferol; Diet; Goats; Male; Milk; Minerals; Zea mays

The effect of defaunating the rumen on growth performance and carcass composition of lambs fed a molasses-urea diet was investigated. Before the growth trial, all the animals were defaunated. Based on live weight and daily gain during a preliminar period, the animals were divided in two groups whereafter one group was refaunated. Defaunation caused a decrease in propionic acid percentage in the rumen. Daily gain and food conversion efficiency were better in the defaunated group, but only during the first five weeks. The response over the whole trial (0-9 weeks) remained positive however. There was a trend towards more meat and less fat in the carcass of defaunated lambs. The fact that two animals died during the defaunation procedure indicates the need for a completely harmless and effective defaunating agent.

Topics: Animal Feed; Animals; Body Composition; Body Weight; Cholecalciferol; Dioctyl Sulfosuccinic Acid; Energy Metabolism; Eukaryota; Fermentation; Male; Molasses; Rumen; Sheep; Urea

It has previously been shown that vitamin D deficiency impairs arginine-induced insulin secretion from the isolated, perfused rat pancreas (Science 1980; 209:823-25). Since vitamin D is known to be metabolized to 1,25-dihydroxyvitamin D3 (1,25[OH]2D3) and 24R,25-dihydroxyvitamin D3 (24,25[OH]2D3), it is essential to clarify which vitamin D metabolite has the important role of enhancing insulin secretion. In this report, a comparison is made of the relative efficacy of 3-wk repletion with vitamin D3 (980 pmol/day), 1,25(OH)2D3 (39 pmol/day or 195 pmol/day), and 24,25(OH)2D3 (650 pmol/day) on arginine-induced insulin secretion from the isolated, perfused rat pancreas; in this experiment, the daily caloric intake of the animals receiving vitamin D or its metabolites was controlled by pair feeding to the caloric intake of the vitamin D-deficient rats. 1,25(OH)2D3 repletion was found to completely restore insulin secretion to the levels seen in vitamin D3-replete, pair-fed controls in both the first and second phases, while 24R,25(OH)2D3 only partially improved insulin secretion, and then only in the first phase. Changes of both serum calcium levels and dietary caloric intake after vitamin D metabolite administration are concluded to play a lesser role on the enhancement of insulin secretion, since, in a separate experiment, vitamin D-deficient rats with normal serum calcium levels did not show recovery of insulin secretion equivalent to the vitamin D-replete animals under conditions of dietary pair feeding. These results suggest that 1,25(OH)2D3 but not 24,25(OH)2D3 plays an essential role in the normal insulin secretion irrespective of the dietary caloric intake and prevailing serum calcium levels.

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Arginine; Body Weight; Calcitriol; Calcium; Cholecalciferol; Dihydroxycholecalciferols; In Vitro Techniques; Insulin; Insulin Secretion; Islets of Langerhans; Male; Perfusion; Rats; Vitamin D Deficiency

Two strains (University of Saskatchewan, white egg and wild type) of mature Japanese quail (Coturnix coturnix japonica), following a 4-week depletion period, were fed one of four diets varying in supplementary vitamin D3: a) no supplementary vitamin D3, b) National Research Council (NRC, 1977) recommended level of 1,200 IU vitamin D3/kg feed, c) 10 times, NRC levels, and d) 100 times NRC levels for 4 weeks. Egg production, egg weight, number of softshelled eggs, body weight, and feed consumption were not affected by vitamin D3 treatment. Hatchability of the white egg strain was not affected by vitamin D3 treatment. Hatchability in the wild type strain was reduced in those birds consuming diets unsupplemented with vitamin D3 although not significantly. Tibia ash was not affected by vitamin D3 treatment. Progeny from hens receiving no supplemental vitamin D3 were smaller throughout a 5-week growth period; however, feed consumption and percentage tibia ash content were similar to those of progeny from the other treatments. Progeny fed 480 IU vitamin D3/kg feed were larger, had higher tibia ash, and similar feed consumption compared with those fed a diet with no added vitamin D3.

Topics: Animals; Body Weight; Cholecalciferol; Coturnix; Eating; Female; Food, Fortified; Male; Oviposition; Quail

The biological activities of free (D3) and sulfoconjugated (SD3) vitamin D3 were compared after 6 weeks of oral administration to D-deficient (-D) female rats which were mated in the meantime. Mothers and pups were sacrificed 1-2 days following parturition and mineral and hormonal plasma status was determined in mothers and bone mineral determinations and bone histomorphometric studies performed. In newborns, plasma levels of Ca, P and 25-hydroxyvitamin D (25(OH)D) were measured. After parturition, -D mothers had decreased body weight (BW) as well as decreased plasma levels of Ca, P and 1,25-dihydroxyvitamin D (1,25(OH)2D) associated with undetectable levels of 25(OH)D. Plasma levels of immunoreactive calcitonin and parathormone, by contrast, were higher than in vitamin D-replete (+D) control mothers. Bone histomorphometric analysis showed osteomalacia and secondary hyperparathyroidism in -D mothers. After parturition, -D +SD mothers had reduced BW compared to D-treated mothers and the plasma parameters measured were abnormal. Almost all bone histomorphometric parameters were found to be intermediate between +D and -D groups without reaching values of +D mothers. By contrast, -D +D mothers had most of the bone formation parameters identical to those of +D mothers. However, bone resorption was still higher while plasma levels of P and 25(OH)D remained slightly, but significantly lower than in +D mothers. In pups, plasma Ca in both D3- and SD3-treated groups was similar to values in +D-treated rats. However, pups from SD3-treated mothers still showed plasma levels of P and 25(OH)D lower than in +D pups. In conclusion, treatment with SD3 in -D mother rats significantly improves the biochemical plasma parameters of pups, but complete normalization can be achieved only in the D3-treated group. Our results show that when administered at equal amounts, SD3 has a much lower biological activity than D3 in -D female rats and cannot therefore replace vitamin D3 particularly during pregnancy.

Topics: Animals; Animals, Newborn; Body Weight; Bone and Bones; Calcifediol; Calcitriol; Calcium; Cholecalciferol; Female; Hyperparathyroidism; Osteomalacia; Parathyroid Hormone; Phosphorus; Pregnancy; Pregnancy Complications; Rats; Vitamin D Deficiency

The relative roles of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D (1,25-(OH)2D) and 24,25-dihydroxyvitamin D (24,25-(OH)2D) in bone mineralization are largely unknown. Young vitamin D depleted rats were fed increasing amounts of vitamin D and grouped radiologically in accordance with the rat line test. They ranged from severely rachitic to normal. Radiology was correlated with serum levels of 25-OHD, 1,25-(OH)2D, 24,25-(OH)2D, ionized calcium, magnesium, and phosphate, with bone histology, and with the total mineral content of the animals. Serum 1,25-(OH)2D rose in a linear fashion to supranormal values during bone healing and correlated with the radiological degree of rickets. Serum 25-OHD was below detection limit in the most rachitic and low in the radiologically normal rats, whereas 24,25-(OH)2D was low in all groups. These two metabolites showed no correlation with the radiologic, histologic or biochemical parameters. In rachitic rats, 1,25-(OH)2D appears to play a major role in bone healing and possibly exerts a direct effect on bone cells. It cannot be ruled out, however, that the effect is mediated through a rise in serum levels of calcium and phosphorus, although signs of bone healing were seen in the presence of a subnormal calcium X phosphorus product. Initiation of mineralization can take place with unmeasurable 25-OHD, and 24,25-(OH)2D seems to be without importance.

Topics: Animals; Body Weight; Bone and Bones; Calcifediol; Calcitriol; Calcium; Cholecalciferol; Magnesium; Organ Size; Phosphorus; Rats; Rats, Inbred Strains; Rickets

The amount of skin calcium-binding protein, evaluated using a sensitive radioimmunoassay and indirect immunofluorescence, was decreased in vitamin-D deficient rats and increased after one week vitamin D3 or 1 alpha-hydroxyvitamin D3 treatment. In vitamin D replete and in vitamin D-deficient animals, skin calcium-binding protein was not sensitive to changes in dietary and/or serum calcium concentrations. These results indicate that this protein is different from other calcium-binding proteins such as parvalbumin and calmodulin which are not vitamin D-dependent, and also different from intestinal calcium-binding protein which, in D replete animals, is sensitive to changes in dietary and serum calcium concentrations. Skin calcium-binding protein may, therefore, represent a new class of vitamin D-dependent protein.

Topics: Animals; Body Weight; Calcium; Calcium-Binding Proteins; Cholecalciferol; Cytosol; Fluorescent Antibody Technique; Kinetics; Male; Radioimmunoassay; Rats; Rats, Inbred Strains; S100 Calcium Binding Protein G; Skin; Vitamin D Deficiency

A study was undertaken to determine the effects of maternal and poult nutrition on poult growth and bone development through to market age. Nicholas Large White turkey hens (200) were fed diets with 300, 900, or 2700 IU vitamin D3/kg from day-old to 37 weeks of age. Male poults (649 from Hatch 1 and 555 from Hatch 2) were fed diets containing .6 or 1.2% Ca; .4 or .8% available P; and 300, 900, or 2700 IU vitamin D3/kg to 4 weeks (Hatch 1) or 2 weeks of age (Hatch 2) in a complete factorial design. All Hatch 2 poults were given a "therapeutic" diet from 2 to 4 weeks, followed by normal grower diets from 4 to 24 weeks of age. Increasing the level of vitamin D3 in the hen diet increased weight at hatching and at 2 and 4 weeks, decreased mortality from 0 to 2 weeks, and increased bone ash percent and breaking strength and decreased the severity of rickets score at 2 weeks. Increasing the levels of Ca, P, and vitamin D3 in the poult diet gave reduced mortality from 0 to 2 weeks, increased weight at 2 and 4 weeks, increased bone ash percent and breaking strength, and decreased severity of rickets score at 2 and 4 weeks. Carcass fleshing score at 24 weeks was improved with 1.2% Ca. Conformation score and percent grade A carcasses increased linearly with level of vitamin D3 in the starter diet and were also improved by increasing the vitamin D3 in the breeder diet.

Topics: Animals; Body Weight; Bone Development; Calcium, Dietary; Cholecalciferol; Female; Male; Phosphorus; Poultry Diseases; Rickets; Turkeys

A comparative study on the amount of goblet cells and excretion of endogenic calcium in the small intestine of chicks has been made. The amount of goblet cells (per brush area unit) significantly increased at the deficiency of vitamin D3 as well as at the surplus of calcium in the diet. Excretion intensity of endogenic calcium (determined by 45Ca) correlates directly with the amount of goblet cells. Histochemical and electron microscopical investigations show that precipitate accumulations containing calcium are absorbed in goblet cells and their secret on the surface of the cells. The significance of goblet cells in the intestinal excretion of endogenic calcium is discussed.

Topics: Animals; Body Weight; Calcium; Calcium Radioisotopes; Chickens; Cholecalciferol; Diet; Histocytochemistry; Intestine, Small; Male; Vitamin D Deficiency

To clarify the role of vitamin D in the regulation of the endocrine pancreas, we have studied insulin and somatostatin secretion in vitamin D deficient rats (reared on a vitamin D deficient diet), D-replete rats (reared on a vitamin D deficient diet and given 160 IU of vitamin D3 sc twice a week) and control rats (reared on laboratory chow), using the isolated perfused rat pancreas. In the vitamin D deficient rats, the perfusate insulin induced by 16.7 mM glucose was only 35% of the secretion in the control rats. In the D-replete rats, the insulin release was restored to that of the controls. Similarly, the plasma insulin level in the vitamin D deficient rats was very low and the level in the D-replete rats was also restored to the level of the controls. The perfusate somatostatin response to glucose was not significantly different in any of the three groups. In addition, since the plasma calcium level in the vitamin D deficient rats was very low and in the D-replete rats was still lower, compared to normal rats, we suggest that vitamin D acts not only via the plasma calcium level but possibly also directly on the B cell.

Topics: Animals; Binding, Competitive; Blood Glucose; Body Weight; Calcifediol; Calcium; Cholecalciferol; Insulin; Insulin Secretion; Islets of Langerhans; Male; Protein Binding; Rats; Rats, Inbred Strains; Somatostatin; Vitamin D Deficiency

The effects of maternal vitamin D3 carry-over to the poult and dietary vitamin D3 on kidney 25-hydroxyvitamin D3-1-hydroxylase (1-hydroxylase) (EC 1.14.13.13) activity were studied in poults from 6 days prehatching to 46 days of age. Large White female turkeys from day-old were fed diets with either 300, 900, or 2700 IU vitamin D3/kg feed. Progeny from each maternal group were fed diets with either 0, 300, 900, or 2700 IU vitamin D3/kg feed. Low maternal vitamin D3 carry-over increased kidney 1-hydroxylase activity in embryos and poults to at least 5 days of age. Low dietary vitamin D3 increased the enzyme activity over that of poults fed higher levels. Kidney 1-hydroxylase activity peaked at about 8 to 18 days to a level similar in all groups. This peak is coincident with the appearance of rickets often noted in the field. Maternal diet did not affect plasma calcium (Ca) but plasma inorganic phosphorus (Pi) decreased with decreasing maternal vitamin D3 up to 14 days of age. Plasma Ca increased at 14 days with higher dietary vitamin D3, as did plasma Pi from day 8. Plasma alkaline phosphatase increased with age to 18 days and then declined. Tibia ash increased with higher maternal vitamin D3 carry-over to 12 days and with higher dietary vitamin D3 after 12 days of age. Body weight was reduced with low maternal vitamin D3 carry-over until at least 2 weeks of age, after which the effect of progeny diet was highly significant; birds receiving 2700 IU vitamin D3/kg feed were almost twice as large as those receiving none. This study shows the importance of adequate maternal carry-over of vitamin D3 and its possible influence on the development of rickets in starting poults.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Body Weight; Bone and Bones; Calcium; Cholecalciferol; Diet; Female; Kidney; Male; Minerals; Poultry Diseases; Rickets; Steroid Hydroxylases; Turkeys

When fed to chicks rye is rachitogenic as well as growth depressing. The component or components of rye that cause these effects have not been identified. In an attempt to separate the factors, a water extract of rye was fractionated by precipitation with ethanol or ammonium sulfate. The precipitated fractions were fed to chicks. Although there were different responses to growth and bone ash from the ethanol fractions, they were not statistically significant. In another experiment, guar gum, pectin, or gum arabic was fed to chicks as 2% of the diet. Guar gum was both growth depressing and rachitogenic, pectin was only growth depressing, and gum arabic was without effect.

Topics: Animals; Body Weight; Chemical Fractionation; Chickens; Cholecalciferol; Dietary Carbohydrates; Dietary Fiber; Edible Grain; Food Additives; Galactans; Gum Arabic; Mannans; Pectins; Plant Gums; Polysaccharides; Poultry Diseases; Rickets; Secale

A demonstration project is described that proved to be popular with undergraduate students enrolled in a senior level course on animal and poultry nutrition. A total of 100 male, day-old broiler chicks were housed in a Petersime battery brooder and used in a 3-week test. Students were responsible for the management and care of the birds throughout the test. The birds were allotted to 5 groups (4 replicates each of 5 birds per group) and the test involved the omission of calcium, phosphorus, vitamin D3, or sodium chloride from a nutritionally adequate diet for a period of 2 weeks. After that period, one pen of each group was repleted with the control diet. Feed consumption, liveweight, feed conversion efficiency, and tibia bone ash content were measured weekly. Deficiency signs of the nutrients were observed, and it was noted that sodium chloride had the most marked effect on growth. Phosphorus deficiency had the most severe effect on bone development and resulted in a high incidence of rickets. Repletion resulted in a marked response in all parameters measured and was most marked in the group deficient in sodium chloride.

Topics: Animals; Body Weight; Bone and Bones; Calcium Carbonate; Calcium Phosphates; Chickens; Cholecalciferol; Diet; Eating; Feeding Behavior; Male; Minerals; Nutrition Disorders; Poultry Diseases; Sodium Chloride

Alterations in circulating vitamin D3 metabolites have been documented in both experimental and human diabetes mellitus. Using a recirculating hepatic perfusion system and in vitro kidney mitochondrial assays, we studied vitamin D3 hydroxylation in control and insulin-deficient rats 6 weeks after the induction of streptozotocin-diabetes. Vitamin D3-25-hydroxylase activity, assessed by hepatic conversion of [3H]vitamin D3 to [3H]25-hydroxyvitamin D3 during a 4-h perfusion, was similar in diabetic and control animals. The hepatic degradation of 25-hydroxyvitamin D3 to more polar metabolites was also normal, as was glucuronide conjugation and biliary excretion of vitamin D3 metabolites. The chronic insulin-deficient state resulted in a significantly (P less than 0.01) decreased 1 alpha-hydroxylase activity and enhanced (P less than 0.001) renal 24-hydroxylase activity. These alterations in vitamin D metabolism may relate to the deranged mineral homeostasis and skeletal morphology observed in rats and humans with chronic insulin deficiency.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Blood Glucose; Body Weight; Cholecalciferol; Cytochrome P-450 Enzyme System; Diabetes Mellitus, Experimental; Kidney; Male; Mitochondria; Rats; Rats, Inbred Strains; Steroid Hydroxylases; Vitamin D Deficiency; Vitamin D3 24-Hydroxylase

The myopathy associated with vitamin D deficiency was examined in vitamin D-deficient and vitamin D-supplemented rats. When compared with either vitamin D-supplemented ad lib. or pair-fed rats, weight gain and muscle mass were decreased in vitamin D-deficient hypocalcemic animals. With the exception of a modest decrease in muscle creatine phosphate levels, muscle composition was unchanged by vitamin D deficiency. Muscle protein turnover rates were determined in both in vivo and in vitro studies and demonstrated that myofibrillar protein degradation was increased in vitamin D deficiency. Normal growth rates could be maintained be feeding the rats vitamin D-deficient diets containing 1.6% calcium, which maintained plasma calcium within the normal range. In addition to its role in maintaining plasma calcium, vitamin D-supplemented rats had significantly higher levels of the anabolic hormone insulin. Vitamin D supplementation may affect muscle protein turnover by preventing hypocalcemia, as well as directly stimulating insulin secretion, rather than by a direct effect within skeletal muscle.

Topics: Animals; Body Weight; Calcium; Cholecalciferol; Insulin; Male; Muscle Proteins; Muscles; Phosphocreatine; Rats; Rats, Inbred Strains; Vitamin D Deficiency

One-day-old chicks were depleted of vitamin D. At 3 weeks their right tibiae, and those of a control group given vitamin D3, were fractured and pinned. After fracture the controls were kept on vitamin D3. Another group was left vitamin D-deficient. The remaining depleted chicks, divided into four groups, were given vitamin D3, 24,25-dihydroxyvitamin D3 [24,25(OH)2D3], 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] or a combination of 24,25(OH)2D3 and 1,25(OH)2D3. The callus obtained after 9 and 14 days was subjected to torsional stress. The callus of chicks given vitamin D continuously showed the greatest resistance, whereas that of vitamin D-deficient chicks showed the smallest resistance. Repletion with either vitamin D3 or its metabolites increased the strength of the callus. Repletion with the combination of 24,25(OH)2D3 and 1,25(OH)2D3 produced the most marked results, in that the callus was even stronger than that of chicks replete with vitamin D3. It is concluded that 24,25(OH)2D3 is essential for bone formation in addition to the known active vitamin D metabolite 1,25(OH)2D3, and the possible clinical implications of these findings are discussed.

Topics: 24,25-Dihydroxyvitamin D 3; Animals; Body Weight; Bony Callus; Calcitriol; Calcium; Chickens; Cholecalciferol; Dihydroxycholecalciferols; Male; Phosphates; Stress, Mechanical; Tibial Fractures; Wound Healing

Two experiments were conducted on dietary predisposition to rickets in poults. The first experiment compared fat type (corn oil or tallow), level of added fat (3.5 or 7%), vitamin D3 (900 or 2,400 IU/kg feed), and total calcium (.6, 1.2, or 3%) inclusion in the diet. Poults fed diets supplemented with corn oil had higher percentage tibia ash than poults fed tallow-supplemented diets. Vitamin D3 included at 2,400 IU/kg feed increased body weights significantly by 2 and 4 weeks of age and lowered plasma alkaline phosphatase (AP) at 2 and 4 weeks compared with diets containing 900 IU/kg feed. Tibia ash was significantly greater with the higher vitamin D3 supplementation at 2 weeks. At 2 weeks of age both low (.6%) and high (3%) levels of dietary calcium increased plasma AP, decreased tibia ash, and decreased body weight compared with diets containing 1.2% calcium. By 4 weeks of age, diets containing 1.2 and 3% calcium had no significant effects on body weight and plasma AP; however, tibia ash was significantly greater with these levels than with the .6% calcium diets. The second experiment compared level of dietary tallow inclusion (2.5 or 7%) and supplementary vitamin A (4,000, 16,000, or 44,000 IU/kg feed). The high tallow diets decreased tibia ash at 3 weeks, and the maximum supplementation of vitamin A significantly depressed body weight. Clinical rickets were first noted at 18 days of age. By 26 days of age the higher level of dietary fat and the highest level of vitamin A caused a significant increase in severity of rickets. The results suggested that rickets can be induced by high dietary levels of tallow and vitamin A.

Topics: Alkaline Phosphatase; Animals; Body Weight; Bone and Bones; Calcium; Calcium, Dietary; Cholecalciferol; Dietary Fats; Disease Susceptibility; Male; Phosphorus; Poultry Diseases; Rickets; Turkeys; Vitamin A

Two experiments were conducted to determine the influence of fat retention on bone mineralization and amino acid retention for broiler chicks fed rye diets containing marginal levels of vitamin D3. In Experiment 1, rye diets containing tallow were supplemented with high vitamin D3, bile salt (sodium taurocholate), or a detergent (sodium lauryl sulphate). Fat retention and tibia ash were improved (P less than .05) with bile salt addition, and tibia ash alone (P less than .05) was improved when high vitamin D3 or the detergent was added to the diet. In Experiment 2, rye diets contained tricaprylin (TC), tristearin (TS), or triolein (TO) as a fat source. Both fat retention (TS less than TO less than TC) and tibia ash (TS less than TC less than TO) showed a significant (P less than .05) treatment effect. The results of both experiments support the hypothesis that the rachitogenic effect of feeding rye may be related to inadequate fat digestion. There was no significant treatment effect on amino acid retention in either experiment. A third experiment indicated a similar bile acid pool size for chicks fed rye as opposed to wheat; however, bile acid concentration of jejunal fluid was lower (P less than .05) for chicks fed rye. A possible microbial involvement in the disturbance of bile acid metabolism was indicated by the capacity of Streptococcus organisms derived from chick small bowel to degrade sodium taurocholate.

Topics: Amino Acids; Animals; Bile Acids and Salts; Body Weight; Bone and Bones; Chickens; Cholecalciferol; Diet; Dietary Fats; Edible Grain; Food Additives; Lipid Metabolism; Male; Minerals; Secale; Sodium Dodecyl Sulfate; Taurocholic Acid; Triticum

Rye has growth-depressing and rachitogenic properties when fed to chicks. Growth depression also is observed when chicks are fed certain polysaccharides, particularly pectin. Rye has about 8% pectin-like material. A commercially available pectic enzyme preparation was fed to chicks at .1% of the rye diet. This enzyme permitted better utilization of rye for growth and also alleviated the rachitogenic effects of rye. The supplemental enzyme permitted maximal bone mineralization with 200 to 300 ICU of vitamin D3/kg diet, whereas 500 ICU/kg otherwise were required with rye diets.

Topics: Animals; Body Weight; Chickens; Cholecalciferol; Diet; Edible Grain; Enzymes; Secale; Zea mays

Topics: Animals; Body Weight; Bone and Bones; Calcifediol; Cholecalciferol; Femur; Hydroxycholecalciferols; Male; Minerals; Rats; Vitamin D Deficiency

Calcitonin and 1.25(OH)2D3 have opposite effects on the serum concentrations of Ca and P, as well as on bone resorption, and can be observed in the process of healing of standardized fracture in adult rats. The rats given 1.25(OH)2D3 had a stronger fracture callus and slightly less pronounced postfracture osteopenia. Calcitonin did not significantly influence the fracture healing but had a pronounced effect in preventing the osteopenia. The effects of 1.25(OH)2D3 are believed to be indirect, i.e., through the changes in the serum Ca X P product, whereas the osteopenia preventing action of calcitonin may come from direct effect on bone.

Topics: Animals; Body Weight; Bony Callus; Calcitonin; Calcium; Cholecalciferol; Femoral Fractures; Male; Phosphorus; Rats; Tensile Strength; Wound Healing

Topics: Alanine Transaminase; Aniline Hydroxylase; Animals; Body Weight; Calcifediol; Cholecalciferol; Cytochrome P-450 Enzyme System; Hydroxycholecalciferols; Liver; Male; Phenobarbital; Phenytoin; Rats; Time Factors

Experimental hypervitaminosis D was produced in rabbits by feeding 25,000 I.U. vitamin D3 or the corresponding amount of vitamin D3 palmitate per kg of diet. Hypercalcemia and hyperphosphatemia was accompanied by increased CaBP activity and reduced weight gain in the vitamin D3 group as well as in the vitamin D3 ester group. The degree of calcification in the aorta and in the kidney also was similar in both groups. Increasing the vitamin intake by giving 10,000 I.U. vitamin D3 or vitamin D3 palmitate per day resulted in earlier and more widespread calcific deposits. In rats, receiving 50,000 I.U. vitamins D3 or vitamin D3 palmitate per kg of diet, calcification in soft tissue was much less extensive than in rabbits. But again, no difference was seen between vitamin D3 and vitamin D3 palmitate. These results indicate, that vitamin D3 esters are not suitable as a less calcinogenic form of vitamin D3.

Topics: Animals; Aorta; Body Weight; Calcinosis; Calcium; Cholecalciferol; Intestinal Mucosa; Kidney; Male; Myocardium; Phosphates; Rabbits; Rats; S100 Calcium Binding Protein G

Decalcified bone matrix was prepared from cortical bones of rats premedicated with I) Diphenylhydantoin (DPH), II) DPH + Vitamin D3, III) Vitamin D3 or IV) no premedication for 10 days. In the donor animals, DPH lowered the serum calcium level, caused a weight loss of 10 per cent, and stopped the growth of the long bones. Vitamin D3 supplementation normalized the serum calcium concentration but had no effect on the other parameters. Vitamin D3 alone caused hypertrophy of the growth cartilage, while the bone growth and structure was normal. The bone inductive capacity of decalcified bone matrix was highest in the DPH group, and the DPH + D3 group also showed significantly higher values than the D3, and control groups. The results of the present study show that the bone inductive capacity of the decalcified bone matrix is independent of Vitamin D3 metabolism.

Topics: Animals; Body Weight; Bone Development; Bone Matrix; Calcium; Cartilage; Cholecalciferol; Hypertrophy; Male; Phenytoin; Rats; Rats, Inbred Strains

Rats maintained on low-protein rachitogenic diets show increased intestinal calcium transport, serum inorganic phosphate and increased endochondral calcification responses to calciferol, 25-hydroxycholecalciferol (25-OH-CC) and 1,25-dihydroxycholecalciferol (1,25-(OH)2CC). Because enhanced responses are observed with 1,25-dihydroxycholecalciferol as well as its precursors, it is unlikely that the effect of dietary protein is mediated by a change in the calciferol-25-hydroxylase and the 25-hydroxycholecalciferol-1 alpha-hydroxylase. Instead, it appears that either metabolism of 1,25-dihydroxycholecalciferol or its activity in the target organs is affected.

Topics: Animals; Body Weight; Bone and Bones; Calcium; Cholecalciferol; Dietary Proteins; Dihydroxycholecalciferols; Hydroxycholecalciferols; Intestinal Absorption; Intestinal Mucosa; Male; Rats; Rickets

Topics: Aminopyrine N-Demethylase; Animals; Body Weight; Cholecalciferol; Cholestanetriol 26-Monooxygenase; Diet; Enzyme Induction; Kinetics; Male; Microsomes, Liver; Mixed Function Oxygenases; Organ Size; Phenobarbital; Proteins; Rats; Steroid Hydroxylases

Topics: Animals; Body Weight; Calcium; Cholecalciferol; Dihydroxycholecalciferols; Hydroxycholecalciferols; Male; Phosphorus; Rats

Topics: Analysis of Variance; Animals; Body Weight; Calcium; Chickens; Cholecalciferol; Dihydroxycholecalciferols; Endocrine Glands; Fertility; Hydroxycholecalciferols; Phosphates

Topics: Animals; Anticonvulsants; Body Weight; Cholecalciferol; Enzyme Induction; Folic Acid; Formiminoglutamic Acid; Liver; Male; Microsomes, Liver; Organ Size; Phenobarbital; Phenylbutyrates; Rats; Urea

Urinary calculi composed of calcium oxalate were produced in male hooded Wistar rats fed a vitamin B6 deficient diet over 16 weeks. This basic diet was modified by doubling the phosphate content or loading with vitamin C or D3 in three treatment groups. The number of rats developing oxalate stones was not altered by the addition of vitamin D3 or phosphate, but there was a significant increase in total weight of stone formed and histological evidence of extensive renal damage in rats on the high vitamin D3 diet. The addition of vitamin C to the vitamin B6 deficient rats resulted in a reduction in the number of rats with uroliths and a fall in urinary oxalate excretion, while similarly loaded vitamin B6 supplemented controls were free of oxalate calculi. It is concluded that the oxalate urolithiasis induced by vitamin B6 deficiency was exacerbated by added vitamin D3 and reduced by vitamin C.

Topics: Animals; Ascorbic Acid; Body Weight; Calcium Oxalate; Cholecalciferol; Diet; Kidney; Male; Phosphates; Pyridoxine; Rats; Urinary Calculi; Vitamin B 6 Deficiency

Topics: Animals; Body Weight; Cholecalciferol; Lethal Dose 50; Liver; Male; Phenobarbital; Phenytoin; Rats

1. Food intake studies were carried out on three groups of captive primates (anthropoid apes (Pongidae), lemurs (Lemuridae) and marmosets (Callitrichidae). 2. Determination and analysis of the nutrient intakes were carried out by calculations based on food tables. The results from all groups were compared. 3. Marmosets were found to have higher intakes of energy and many other nutrients than the apes and lemurs. 4. The results suggest that there is a tendency towards over use of dietary supplements and foods of higher nutrient density for captive primates.

Topics: Animal Nutritional Physiological Phenomena; Animals; Animals, Zoo; Body Weight; Calcium; Callitrichinae; Cholecalciferol; Diet; Dietary Fats; Dietary Proteins; Female; Haplorhini; Hominidae; Lemur; Male; Phosphorus; Primates; Vitamin A

Florid rickets developed in chicks receiving doses of diphenylhydantoin analogous to doses used in humans as anticonvulsants, vitamin D3 being given in amounts sufficient for normal bone mineralization in controls. The changes in the bones were directly related to the dose of diphenylhydantoin and inversely related to the dose of vitamin D3. Bone mineralization was assessed by roentgenography, histological examination, microradiography, and measurement of bone ash. Of these methods, roentgenography was the least sensitive. Rachitic changes were detectable by light microscopy and microradiography in chicks whose skeletons appeared normal roentgenographically. Roentgenographic evidence of rickets became detectable only when the rickets was far advanced. Rickets developed at serum levels of diphenylhydantoin similar to those found in patients taking anticonvulsant medication.

Topics: Animals; Body Weight; Bone and Bones; Cholecalciferol; Male; Microradiography; Nutritional Requirements; Phenytoin; Rickets

Topics: Age Factors; Animals; Biological Availability; Body Weight; Chickens; Cholecalciferol; Fluorides; Hydroxycholecalciferols; Male; Phosphorus; Toes

25-Hydroxyvitamin D (25-OHD) levels were measured in 39 patients with metabolic bone disease or hypoparathyroidism who had been treated with a constant high dose of vitamin D2 or D3 for at least 12 weeks. Plasma 25-OHD levels rose with increasing dosage, the relationship between dose and plasma level being approximately linear whether or not the dose was expressed on a weight-corrected basis. A therapeutic range of 25-OHD to be expected when patients with these conditions are treated with vitamin D has been established. There may be certain exceptions in which plasma 25-OHD levels within the range are associated with either an inadequate response to treatment or, conversely, the hypercalcaemia of vitamin D toxicity. There was no correlation between plasma calcium level and 25-OHD concentration in the group of patients studied. There was also no difference between the dose/25-OHD relationship of patients treated with vitamin D2 and that of patients receiving vitamin D3. Ten patients were started on treatment with large doses of vitamin D during the period of the study. The rate of rise of plasma 25-OHD was followed during treatment. The incremental rise in 25-OHD was calculated at the end of the first week of treatment in terms of dose per unit body weight. The rate of rise of plasma 25-OHD level was highly correlated with the dose used. Plasma 25-OHD levels after one weeks' treatment were only 15-20% of the expected steady-state level on the same dosage. The importance of a high priming dose when a rapid response is needed is thus emphasised.

Topics: Adolescent; Adult; Aged; Body Weight; Bone Diseases; Child; Child, Preschool; Cholecalciferol; Dose-Response Relationship, Drug; Ergocalciferols; Female; Humans; Hydroxycholecalciferols; Hypercalcemia; Hypoparathyroidism; Infant; Male; Middle Aged; Vitamin D

The relative toxicity and metabolic effectiveness of cholecalciferol (CC) and 25-hydroxycholecalciferol (25-HCC) in chicks were evaluated by feeding six graded levels of each and observing gross and microscopic pathology as well as several metabolic parameters of calcium metabolism. Renal tubular calcification was observed when CC was fed at the rate of 10.0 mg/kg of diet and when 25-HCC was fed at the rate of 0.1 mg/kg diet. Thus, 100-fold increase in toxicity results when the hydroxylated form of CC is fed. Both microscopic renal lesions and increased renal calcium and inorganic phosphate concentrations occurred in chicks with normal serum calcium concentrations.

Topics: Alkaline Phosphatase; Animals; Body Weight; Calcinosis; Calcium; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Hydroxycholecalciferols; Kidney; Kidney Diseases; Kidney Tubules; Phosphorus

Topics: Animal Feed; Animals; Body Weight; Bone Resorption; Calcium; Calcium, Dietary; Chickens; Cholecalciferol; Egg Shell; Female; Intestinal Absorption; Intestine, Small; Oviposition; Paralysis; Parathyroid Glands; Phosphorus; Poultry Diseases; Protein Binding; Uterus; Vitamin D Deficiency

A comparative study of the effects of vitamin D3 and of a partially purified extract of Solanum malacoxylon has been carried out in rachitic chicks. Vitamin D3 and Solanum malacoxylon increased intestinal calcium absorption and serum calcium levels. They normalized the bone water and ash content. Vitamin D3 produced an increase of serum phosphate while Solanum malacoxylon further decreased the already low phosphate values. Vitamin D3 significantly increased the body weight increment of rachitic chicks, but Solanum malacoxylon did not. It appears that Solanum malacoxylon duplicates certain actions of vitamin D but lacks its phosphate-regulating and growth-promoting actions.

Topics: Alkaline Phosphatase; Animals; Body Weight; Bone and Bones; Calcium; Chickens; Cholecalciferol; Intestinal Absorption; Phosphates; Rickets; Solanaceous Alkaloids; Water

Topics: Animal Feed; Animals; Body Weight; Cholecalciferol; Drug Interactions; Feces; Female; Magnesium; Male; Potassium; Sodium; Turkeys

Three experiments were conducted with Large White turkeys to four weeks of age. The interrelationship of zinc and vitamin D3 was studied in two experiments. Iron and vitamin D3 were involved in one experiment. One group of ten male and one group of ten female poults were randomly assigned to each treatment within an experiment. All experiments involved a factorial arrangement of two dietary variables, D3 and either zinc or iron. For example, all possible combinations of four zinc levels; 31, 46, 76 and 106 p.p.m. and three vitamin D3 levels; 600, 1200, and 3600 I.C. units/kg. were fed in the second zinc experiment. Significant (P less than 0.05) weight gain differences occurred among both zinc and D3 levels in this experiment. Four week body weights were 356, 436, 459 and 444 g., respectively, for Zn levels; and 409, 410 and 452 g., respectively, for D3 levels. Significant (P less than 0.05) interactions occurred between dietary zinc and D3 levels, and between iron and D3 levels relative to body weight gain, Vitamin D3 tended to increase tibia zinc levels in poults receiving higher zinc levels; the opposite occurred with lower levels of the element. Zinc level in feces was decreased with vitamin D3. Hemoglobin level was not influenced by D3 but was increased by iron.

Topics: Animal Feed; Animals; Body Weight; Cholecalciferol; Drug Interactions; Feces; Female; Hemoglobins; Iron; Male; Tibia; Turkeys; Zinc

Topics: Animals; Body Weight; Calcium, Dietary; Chickens; Cholecalciferol; Hydroxycholecalciferols; Male; Nutritional Requirements; Phosphorus; Tibia

Topics: Alkaline Phosphatase; Animals; Body Weight; Calcium; Cholecalciferol; Connective Tissue; Dentinogenesis; Female; Isoniazid; Liver; Male; Microsomes, Liver; Odontogenesis; Organ Size; Phenobarbital; Phenytoin; Phosphates; Rats; Sex Factors

The ability of 24R, 25- and 24S, 25-dihydroxycholecalciferol to stimulate intestinal calcium transport and bone calcium mobilization in chicks was measured. Enhancement of intestinal calcium transport by 325 or 130 nmoles of either compound was maximal by 24 hours. The effects of these compounds on bone calcium mobilization were also maximal by 24 to 36 hours. When lower doses were tested, 2 nmoles of the 24R, 25-dihydroxycholecalciferol significantly stimulated intestinal calcium transport, whereas 130 nmoles of the S isomer were required for a significant response. Neither steroid had a significant effect on bone calcium mobilization when doses of less than 130 nmoles were given. When chicks received orally 32.5, 325 or 1,625 pmoles of 24R, 25-dihydroxycholecalciferol daily from hatching for 4 weeks, several parameters showed a dose-related response. These included growth, serum calcium, bone ash, renal 25-hydroxycholecalciferol-1-hydroxylase and intestinal vitamin D-dependent calcium binding protein. Rats given 32.5 to 1,625 pmoles of 24R, 25-dihydroxycholecalciferol for 3 or 6 weeks were equivalent to vitamin D-treated controls in terms of growth and serum calcium levels. It is concluded that within the lower dose ranges (2 to 30 pmoles) the R isomer of 24,25-dihydroxycholecalciferol is more active in stimulating intestinal calcium transport than the S isomer but that neither compound increases bone calcium mobilization at these dose levels. Also, the rat is more responsive in terms of growth and serum calcium, to small dialy doses of 24R, 25-dihydroxycholecalciferol than is the chick.

Topics: 25-Hydroxyvitamin D3 1-alpha-Hydroxylase; Animals; Biological Transport; Body Weight; Bone and Bones; Calcium; Chickens; Cholecalciferol; Dihydroxycholecalciferols; Hydroxycholecalciferols; Intestines; Kidney; Male; Minerals; Phosphorus; Protein Binding; Rats; Species Specificity; Stereoisomerism; Structure-Activity Relationship

We studied diabetic rats, 5 days after streptozotocin injection, and matched controls to determine whether depressed duodenal calcium absorption associated with uncontrolled diabetes in the rat would respond to vitamin D or its metabolites. At the appropriate time following the intravenous injection of 0.25 mug of either vitamin D3, 25-hydroxycholecalciferol (25-OHD3), 1,25-dihydroxycholecalciferol (1,25-OH)2D3), or 1alpha-hydroxycholecalciferol (1alpha-OHD3) to half of each diabetic and control group, calcium transport was evaluated using everted duodenal sacs with 0.4 mM40Ca and tracer 45Ca on both mucosal and serosal surfaces. All agents stimulated duodenal calcium absorption in controls. Diabetics responded only to 1,25-(OH)2D3, the metabolite that acts directly on the duodenum, and to its synthetic analog, 1alpha-OHD3. 1alpha-OHD3 is activated to 1,25-(OH)2D3 by 25-hydroxylation in the liver; 25-OHD3 must be 1alpha-hydroxylated in the kidney to be active. The stimulation of duodenal calcium absorption in diabetic rats by 1alpha-OHD3, but not by either vitamin D3 or 25-OHD3, is most consistent with a defect in vitamin D metabolism at the 1alpha-hydroxylation step in the kidney.

Topics: Animals; Body Weight; Calcium; Cholecalciferol; Diabetes Mellitus; Dihydroxycholecalciferols; Duodenum; Gastric Mucosa; Hydroxycholecalciferols; Intestinal Absorption; Male; Rats; Streptozocin

Three experiments using day-old chicks were conducted in battery brooders to further study the rye-vitamin D antagonism. Birds were fed a vitamin D3-free diet containing corn or rye and submitted to diverse treatments for the first 10 days. At this time the chicks were either continued on the same diet or changed to other grain-type diets. The effect of ultraviolet light exposure on the chicks and of a single oral dose of vitamin D3 was studied, and body weight gain and bone ash were determined after a one-week experimental period. Rachitic chicks on a corn diet responded significantly better than rye-fed chicks to a single oral dose of vitamin D3, based on bone ash of fat-free, dry tibia. This rachitogenic effect of rye was completely overcome by exposing the chicks to ultraviolet light or by water extraction or acid-autoclaving this grain. The results also demonstrate that the interference by rye does not persist after this grain is removed from the diet.

Topics: Administration, Oral; Animal Feed; Animals; Body Weight; Chickens; Cholecalciferol; Edible Grain; Female; Male; Poultry Diseases; Rickets; Secale; Tibia; Ultraviolet Rays; Zea mays

Topics: Animals; Biological Transport; Body Weight; Bone and Bones; Calcium; Cholecalciferol; Hydroxycholecalciferols; Intestinal Absorption; Male; Rats; Vitamin D Deficiency

Groups of lambs were fed four levels of a diet based upon oaten grain. Two groups gained weight rapidly, one less rapidly and the other lost liveweight over a 32-day period. Serum alkaline phosphatase activity was found to be closely correlated to liveweight, in a positive linear manner, in those lambs gaining weight rapidly. This relationship was similar in lambs of R or r blood group. Supplementation of the diet with limestone and or sodium chloride did not influence the relationship. This relationship is considered to reflect the influence of the dietary treatments upon the rate of skeletal metabolism.

Topics: Alkaline Phosphatase; Animal Feed; Animals; Aspartate Aminotransferases; Blood Proteins; Body Weight; Calcium; Cholecalciferol; Creatine Kinase; Edible Grain; Fatty Acids, Nonesterified; Injections, Subcutaneous; L-Lactate Dehydrogenase; Magnesium; Male; Ornithine Carbamoyltransferase; Phosphorus; Poaceae; Sheep; Vitamin A

Rickets, hypocalcemia, decreased duodenal calcium transport, and reduction of calcium binding protein have been produced in chicks treated with diphenylhydantoin. These effects are directly related to diphenylhydantoin dose and inversely related to the intake of vitamin D(3) (cholecalciferol).

Topics: Animals; Body Weight; Bone and Bones; Calcium; Calcium Radioisotopes; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Duodenum; Hypocalcemia; Intestinal Mucosa; Male; Phenytoin; Protein Binding; Rickets; Vitamin D Deficiency

Topics: Animals; Body Weight; Bone and Bones; Calcium; Chickens; Cholecalciferol; Diet; Growth; Hydroxycholecalciferols; Kidney; Male; Mixed Function Oxygenases; Phosphorus; Radiography; Rickets

Topics: Animals; Body Weight; Cholecalciferol; Dwarfism; Female; Growth; Maternal-Fetal Exchange; Pentobarbital; Phenytoin; Pregnancy; Rats; Time Factors

Topics: Animal Nutritional Physiological Phenomena; Animals; Body Weight; Bone and Bones; Bone Development; Calcium; Chickens; Cholecalciferol; Dose-Response Relationship, Drug; Elements; Femur; Hypocalcemia; Magnesium; Male; Organ Size; Phosphates; Vitamin D Deficiency

Topics: Acute Disease; Administration, Oral; Albuminuria; Animals; Body Weight; Cadmium Poisoning; Cholecalciferol; Female; Hydroxycholecalciferols; Kidney; Liver; Male; Mice; Mice, Inbred ICR; Organ Size; Skinfold Thickness

Topics: Animals; Anticonvulsants; Avitaminosis; Body Weight; Calcium; Calcium Radioisotopes; Cholecalciferol; Enzyme Induction; Epilepsy; Humans; Hypocalcemia; Intestinal Absorption; Liver; Long-Term Care; Mice; Osteomalacia; Phenobarbital; Phenytoin; Rats; Vitamin D

Topics: Animals; Body Weight; Calcification, Physiologic; Calcium; Cholecalciferol; Diet; Male; Phosphorus; Rats

Topics: Animal Nutritional Physiological Phenomena; Animals; Body Weight; Bone and Bones; Calcium; Chickens; Cholecalciferol; Dihydroxycholecalciferols; Dose-Response Relationship, Drug; Hydroxycholecalciferols; Male; Minerals; Rickets; Tibia

Topics: Alkaline Phosphatase; Animal Nutritional Physiological Phenomena; Animals; Biological Assay; Body Weight; Bone and Bones; Bone Development; Cholecalciferol; Dose-Response Relationship, Drug; Evaluation Studies as Topic; Femur; Hindlimb; Male; Minerals; Phosphorus; Turkeys; Vitamin D Deficiency

Topics: Administration, Topical; Alkaline Phosphatase; Animals; Benz(a)Anthracenes; Body Weight; Calcium; Carcinoma, Squamous Cell; Cell Membrane; Cell Membrane Permeability; Cheek; Cholecalciferol; Cricetinae; Ergocalciferols; Male; Models, Biological; Mouth Mucosa; Mouth Neoplasms; Neoplasms, Experimental; Protein Binding; Spectrophotometry

Topics: Animal Nutritional Physiological Phenomena; Animals; Body Weight; Bone and Bones; Calcium; Calcium Isotopes; Cholecalciferol; Deficiency Diseases; Hydroxycholecalciferols; Hypercalcemia; Intestinal Mucosa; Intestine, Small; Kidney; Lipid Metabolism; Liver; Male; Osteomalacia; Phosphorus; Rats; Rickets; Tritium; Urine

Topics: Adult; Alkaline Phosphatase; Body Height; Body Weight; Calcium; Child, Preschool; Cholecalciferol; Ergocalciferols; Female; Humans; Hydroxyproline; Hypophosphatemia, Familial; Male; Osteomalacia; Phosphates; Phosphorus; Radiography; Wrist

Topics: Age Factors; Animal Nutritional Physiological Phenomena; Animals; Biological Assay; Body Weight; Bone and Bones; Calcium; Calcium Isotopes; Chickens; Cholecalciferol; Evaluation Studies as Topic; Hydroxycholecalciferols; Intestinal Absorption; Male; Minerals; Rats; Rickets; Species Specificity; Time Factors; Tritium

Topics: Alkaline Phosphatase; Alpha-Globulins; Animals; Biological Transport; Biopsy; Blood Proteins; Body Weight; Calcium; Carbon Isotopes; Centrifugation; Cholecalciferol; Chromatography, DEAE-Cellulose; Chromatography, Gel; Diet; Electrophoresis, Disc; Ergocalciferols; Haplorhini; Immunoelectrophoresis; Lipoproteins; Male; Methods; Nutritional Requirements; Phosphorus; Protein Binding; Ribs; Serum Albumin; Spectrum Analysis; Vitamin D; Vitamin D Deficiency

Topics: Animal Feed; Animals; Body Weight; Calcification, Physiologic; Calcium; Chickens; Cholecalciferol; Eggs; Female; Food Additives

Topics: Age Factors; Alkaline Phosphatase; Analysis of Variance; Animals; Body Weight; Bone and Bones; Calcium; Chickens; Cholecalciferol; Diet; Drug Interactions; Female; Intestinal Mucosa; Male; Phosphorus; Sex Factors

Tritiated 1,25-dihydroxycholecalciferol accumulates in several tissues, to an extent that varies with dietary calcium content, 12 hr after the administration of 325 pmoles of tritiated 25-hydroxycholecalciferol to rats. As the dietary and serum calcium concentrations increase, the amount of 1,25-dihydroxycholecalciferol is diminished and the concentration of 21,25-dihydroxycholecalciferol increases. This correlation is especially evident in rats given vitamin D(3). In vitamin D-deficient rats, the repression of 1,25-dihydroxycholecalciferol formation occurs with a diet containing 3% calcium and 20% lactose. The results suggest that the production of 1,25-dihydroxycholecalciferol, believed to be the metabolically active form of vitamin D in the intestine, is responsible for the adaptation of calcium absorption to low dietary concentrations of calcium.

Topics: Animals; Autoradiography; Body Weight; Bone and Bones; Calcium; Calcium, Dietary; Cholecalciferol; Chromatography, Ion Exchange; Hydroxycholecalciferols; Intestinal Mucosa; Kidney; Male; Phosphorus; Rats; Spectrum Analysis; Time Factors; Tritium; Vitamin D Deficiency

Topics: Animals; Body Weight; Bone Development; Calcification, Physiologic; Calcium; Calcium, Dietary; Chickens; Cholecalciferol; Diet; Male; Nutritional Requirements; Strontium; Vitamin D

Topics: Animals; Body Weight; Calcium; Chickens; Cholecalciferol; Chromatography, Gas; Chromatography, Thin Layer; Ergocalciferols; Ketones; Methods; Oxidation-Reduction; Plant Extracts; Plants; Rickets; Spectrum Analysis; Sterols; Vitamin D; Zea mays

Topics: Animals; Body Weight; Calcium; Calcium Chloride; Cholecalciferol; Dogs; Female; Hypercalcemia; Injections, Intramuscular; Male; Microscopy, Electron; Mitosis; Parathyroid Glands; Thyroid Gland; Time Factors

Topics: Animals; Body Weight; Calcium; Cholecalciferol; Diarrhea

Topics: Animals; Biological Assay; Body Weight; Bone and Bones; Chickens; Cholecalciferol; Chromatography; Radiation Effects; Rats; Rickets; Skin; Sterols; Ultraviolet Rays

Topics: Alkaline Phosphatase; Animal Nutritional Physiological Phenomena; Animals; Body Weight; Calcium; Cholecalciferol; Dietary Proteins; Glucose; Glycine max; Phosphates; Rickets; Sterilization; Tibia; Turkeys

Topics: Animals; Body Weight; Bone and Bones; Calcium; Chickens; Cholecalciferol; Dichlorodiphenyldichloroethane; Dihydrotachysterol; Ergocalciferols; Liver; Male; Phosphorus; Rickets; Tibia; Vitamin D

Topics: Animals; Body Weight; Calcium Carbonate; Cholecalciferol; Diet; Ergocalciferols; Female; Growth; Male; Rats; Stimulation, Chemical; Vitamin D

Topics: Animals; Body Weight; Calcinosis; Cholecalciferol; Female; Kyphosis; Lordosis; Rats

Topics: Age Determination by Skeleton; Animals; Blood Chemical Analysis; Body Weight; Calcium; Calcium, Dietary; Caseins; Chlorides; Cholecalciferol; Diet; Glucose; Growth; Magnesium; Minerals; Pharmacology; Phosphates; Phosphorus; Research; Sulfates; Swine; Tetany; Toxicology

Topics: Alkaline Phosphatase; Animals; Avitaminosis; Body Weight; Bone and Bones; Cholecalciferol; Citrates; Diet; Nutrition Disorders; Phosphorus; Phosphorus, Dietary; Rats; Rats, Sprague-Dawley; Research; Rickets; Ultraviolet Rays