leptin and Vitamin-D-Deficiency

Vitamin D deficiency has become an increasing focus of clinical interest, especially in understanding its associations with obesity in adults. The pathological associations linking the two appear to demonstrate complex cellular inflammatory, hormonal and genetic pathways. Enhanced understanding at both microcellular and clinical levels will help clarify the role of obesity in the development of vitamin D deficiency.

Topics: Adiponectin; Adipose Tissue; Cytokines; Humans; Leptin; Obesity; Vitamin D Deficiency

Micronutrient deficiencies have been found in obese individuals across age groups worldwide. While the effects of micronutrient deficiencies on human functions have been studied widely in different populations, there is limited information on how these micronutrient deficiencies affect obese populations. An examination of the available literature suggests associations exist between micronutrient deficiencies and obesity in different populations. These associations and possible mechanisms of the deficiencies' metabolic effects, such as their influence on leptin and insulin metabolism, are discussed here. Further studies are needed to clarify the roles of the different micronutrient deficiencies with respect to obesity and its comorbid conditions.

Topics: Adipose Tissue; Animals; Antioxidants; Calcium; Female; Humans; Insulin; Iron; Iron Deficiencies; Leptin; Male; Micronutrients; Nutritional Status; Obesity; Vitamin A; Vitamin A Deficiency; Vitamin D; Vitamin D Deficiency; Zinc

Osteoporosis is a disorder in which loss of bone strength leads to fragility fractures. This review examines the fundamental pathogenetic mechanisms underlying this disorder, which include: (a) failure to achieve a skeleton of optimal strength during growth and development; (b) excessive bone resorption resulting in loss of bone mass and disruption of architecture; and (c) failure to replace lost bone due to defects in bone formation. Estrogen deficiency is known to play a critical role in the development of osteoporosis, while calcium and vitamin D deficiencies and secondary hyperparathyroidism also contribute. There are multiple mechanisms underlying the regulation of bone remodeling, and these involve not only the osteoblastic and osteoclastic cell lineages but also other marrow cells, in addition to the interaction of systemic hormones, local cytokines, growth factors, and transcription factors. Polymorphisms of a large number of genes have been associated with differences in bone mass and fragility. It is now possible to diagnose osteoporosis, assess fracture risk, and reduce that risk with antiresorptive or other available therapies. However, new and more effective approaches are likely to emerge from a better understanding of the regulators of bone cell function.

Topics: Animals; Bone and Bones; Bone Density; Bone Remodeling; Calcium; Cell Differentiation; Collagen; Estrogens; Fractures, Bone; Glycoproteins; Hematopoietic Stem Cells; Hormones; Humans; Leptin; Ligands; Mice; Models, Biological; Neurons; NF-kappa B; Nitric Oxide; Osteoblasts; Osteoporosis; Osteoporosis, Postmenopausal; Osteoprotegerin; Parathyroid Hormone; Prostaglandins; Receptors, Cytoplasmic and Nuclear; Receptors, Tumor Necrosis Factor; Vitamin D; Vitamin D Deficiency

Topics: Adolescent; Adrenergic beta-Antagonists; Animals; Bone and Bones; Bone Density; Bone Diseases; Child; Dietary Supplements; Diphosphonates; Humans; Leptin; Osteoblasts; Osteogenesis; Pamidronate; Sympathetic Nervous System; Vitamin D; Vitamin D Deficiency

Vitamin D deficiency is a common finding in overweight/obese pregnant women and is associated with increased risk for adverse pregnancy outcome. Both maternal vitamin D deficiency and maternal obesity contribute to metabolic derangements in pregnancy. We aimed to assess the effects of vitamin D3 supplementation in pregnancy versus placebo on maternal and fetal lipids. Main inclusion criteria were: women <20 weeks’ gestation, BMI ≥ 29 kg/m2. Eligible women (n = 154) were randomized to receive vitamin D3 (1600 IU/day) or placebo. Assessments were performed <20, 24−28 and 35−37 weeks and at birth. Linear regression models were used to assess effects of vitamin D on maternal and cord blood lipids. In the vitamin D group significantly higher total 25-OHD and 25-OHD3 levels were found in maternal and cord blood compared with placebo. Adjusted regression models did not reveal any differences in triglycerides, LDL-C, HDL-C, free fatty acids, ketone bodies or leptin between groups. Neonatal sum of skinfolds was comparable between the two groups, but correlated positively with cord blood 25-OH-D3 (r = 0.34, p = 0.012). Vitamin D supplementation in pregnancy increases maternal and cord blood vitamin D significantly resulting in high rates of vitamin D sufficiency. Maternal and cord blood lipid parameters were unaffected by Vitamin D3 supplementation.

Topics: Body Fat Distribution; Cholecalciferol; Cholesterol, LDL; Diabetes, Gestational; Dietary Supplements; Fatty Acids, Nonesterified; Female; Humans; Infant, Newborn; Ketone Bodies; Leptin; Life Style; Obesity; Overweight; Pregnancy; Pregnancy Outcome; Pregnant Women; Triglycerides; Vitamin D; Vitamin D Deficiency; Vitamins

The objective of this article is to evaluate the potential effects of beta-glucan and vitamin D supplementation in patients with diabetic retinopathy. We evaluated the levels of several parameters of inflammatory reactions (C-reactive protein [CRP], serum amyloid A [SAA], and interleukin- [IL-] 6), leptin, and vitamin D. Using a 3-month interval, we divided the patients into three groups: (1) supplemented with beta-glucan and vitamin D, (2) supplemented with vitamin D and placebo, and (3) supplemented with vitamin D alone. By this division, we aim not only to observe whether beta-glucan can increase the effects of vitamin D, but also to eliminate the potential effects of placebo. The doses of vitamin D corresponded to phototype, weight, age, and sex of the individual. Fifty-two diabetic retinopathy patients were selected for our study. We found significant vitamin D deficits in all cases, even after three months of supplementation with vitamin D. Significant changes in levels of CRP were observed in the beta-glucan-supplemented group; levels of SAA and IL-6 were not changed. Leptin levels were significantly lowered in the beta-glucan-supplemented group and increased in the other groups. More detailed studies and/or longer supplementation is necessary.

Topics: Aged; Aged, 80 and over; beta-Glucans; Body Mass Index; C-Reactive Protein; Czech Republic; Diabetic Retinopathy; Female; Humans; Inflammation; Interleukin-6; Leptin; Male; Middle Aged; Placebos; Serum Amyloid A Protein; Vitamin D; Vitamin D Deficiency

Observational studies have suggested that 25-hydroxyvitamin D (25(OH)D) levels are associated with inflammatory markers. Most trials reporting significant associations between vitamin D intake and inflammatory markers used specific patient groups. Thus, we aimed to determine the effect of supplementary vitamin D using secondary data from a population-based, randomised, placebo-controlled, double-blind trial (Pilot D-Health trial 2010/0423). Participants were 60- to 84-year-old residents of one of the four eastern states of Australia. They were randomly selected from the electoral roll and were randomised to one of three trial arms: placebo (n 214), 750 μg (n 215) or 1500 μg (n 215) vitamin D3, each taken once per month for 12 months. Post-intervention blood samples for the analysis of C-reactive protein (CRP), IL-6, IL-10, leptin and adiponectin levels were available for 613 participants. Associations between intervention group and biomarker levels were evaluated using quantile regression. There were no statistically significant differences in distributions of CRP, leptin, adiponectin, leptin:adiponectin ratio or IL-10 levels between the placebo group and either supplemented group. The 75th percentile IL-6 level was 2·8 pg/ml higher (95 % CI 0·4, 5·8 pg/ml) in the 1500 μg group than in the placebo group (75th percentiles:11·0 v. 8·2 pg/ml), with a somewhat smaller, non-significant difference in 75th percentiles between the 750 μg and placebo groups. Despite large differences in serum 25(OH)D levels between the three groups after 12 months of supplementation, we found little evidence of an effect of vitamin D supplementation on cytokine or adipokine levels, with the possible exception of IL-6.

Topics: Adipokines; Adiponectin; Aged; Biomarkers; C-Reactive Protein; Cholecalciferol; Cytokines; Dietary Supplements; Double-Blind Method; Female; Humans; Inflammation; Interleukin-10; Interleukin-6; Leptin; Male; Middle Aged; Vitamin D; Vitamin D Deficiency; Vitamins

Obese adolescents are at a greater risk of vitamin D deficiency because vitamin D is thought to be sequestered by excess adipose tissue. Poor vitamin D status has been associated with a higher prevalence of the metabolic syndrome, type 2 diabetes, or both in adults and adolescents.. The objective was to determine in obese adolescents the efficacy and safety of 4000 IU vitamin D3/d and whether subsequent increased circulating concentrations of 25-hydroxyvitamin D [25(OH)D] are associated with improved markers of insulin sensitivity and resistance and reduced inflammation.. Obese adolescent patients [n = 35; mean ± SD age: 14.1 ± 2.8 y; BMI (in kg/m(2)): 39.8 ± 6.1; 25(OH)D: 19.6 ± 7.1 ng/mL] were recruited from the University of Missouri Adolescent Diabetes and Obesity Clinic and were randomly assigned to receive either vitamin D3 (4000 IU/d) or placebo as part of their standard care. Anthropometric measurements, inflammatory markers (IL-6, TNF-α, C-reactive protein), adipokines (leptin, adiponectin), fasting glucose, fasting insulin, and HOMA-IR values were measured at baseline and at 2 follow-up visits (3 and 6 mo).. After 6 mo, there were no significant differences in BMI, serum inflammatory markers, or plasma glucose concentrations between groups. Participants supplemented with vitamin D3 had increases in serum 25(OH)D concentrations (19.5 compared with 2.8 ng/mL for placebo; P < 0.001), fasting insulin (-6.5 compared with +1.2 μU/mL for placebo; P = 0.026), HOMA-IR (-1.363 compared with +0.27 for placebo; P = 0.033), and leptin-to-adiponectin ratio (-1.41 compared with +0.10 for placebo; P = 0.045). Inflammatory markers remained unchanged.. The correction of poor vitamin D status through dietary supplementation may be an effective addition to the standard treatment of obesity and its associated insulin resistance. This trial was registered at clinicaltrials.gov as NCT00994396.

Topics: Adipokines; Adiponectin; Adolescent; Blood Glucose; Body Mass Index; Child; Cholecalciferol; Dietary Supplements; Female; Humans; Inflammation Mediators; Insulin; Insulin Resistance; Leptin; Male; Obesity; Treatment Outcome; Vitamin D; Vitamin D Deficiency; Vitamins

Hypovitaminosis D has been associated with an increased prevalence of Type 2 diabetes mellitus (DMT2) and metabolic syndrome manifestations. The purpose of this study was to examine the association between 25-hydroxy-vitamin D (25-OH-VitD) levels and indices of insulin resistance (IR), including adipocytokines, in a Saudi population with or without DMT2.. A total of 266 subjects (153 DMT2 and 113 healthy controls) aged 26-80 yr were randomly selected from the existing Biomarkers Screening in Riyadh Program (RIYADH Cohort). Subjects were assessed clinically, anthropometry was performed, morning blood chemistries, including fasting glucose (FG), triglycerides, total cholesterol, LDL cholesterol (LDL-C), and HDL cholesterol were obtained. Homeostasis model assessment of IR (HOMA-IR) was calculated, and serum 25-OH-VitD, leptin, adiponectin, resistin, insulin, high sensitivity CRP (hsCRP), and tumor necrosis factor α concentrations were measured using specific assays.. In DMT2 subjects, negative correlations between 25-OH-vitD and body mass index (BMI), FG, insulin, HOMA-IR, cholesterol, LDL-C, and hsCRP were observed, while a positive correlation between 25-OH-VitD and adiponectin was detected. The later remained significant after controlling for BMI. Interestingly, only weak and nonsignificant associations between 25-OH-VitD and metabolic parameters were observed in the control group, whereas, when the entire population was examined, negative correlations were evident primarily between 25-OH-VitD and FG, HOMA-IR, total cholesterol, LDL-C. These associations remained significant after controlling for BMI.. These results suggest that hypovitaminosis D associations with metabolic disturbances are accentuated in DMT2. The BMIindependent positive correlation between 25-OH-VitD and adiponectin suggests a potential role for this adipocytokine as a link between 25-OH-VitD and IR in patients with DMT2.

Topics: Adipokines; Adiponectin; Adult; Aged; Aged, 80 and over; Body Mass Index; Case-Control Studies; Diabetes Mellitus, Type 2; Female; Humans; Insulin; Insulin Resistance; Leptin; Male; Middle Aged; Prognosis; Vitamin D; Vitamin D Deficiency; Young Adult

Vitamin D deficiency and adipocytokines have been implicated in the etiology of aging-related diseases such as cancer, osteoporosis, and diseases of the cardiovascular system. The association between elevated parathyroid hormone (PTH) and low 25-hydroxyvitamin D (25-OH-VitD) in plasma is used to define vitamin D deficiency, yet their associated mechanistic pathways are unclear. Utilizing plasma samples from women in a previous intervention study, we measured plasma 25-OH-VitD, leptin, adiponectin, PTH, and lipid levels. We observed strong positive associations for leptin with PTH, gamma -tocopherol, and body mass index (BMI) and inverse associations with 25-OH-VitD and adiponectin. Although commonly accepted that vitamin D deficiency causes hyperparathyroidism, we observed this association primarily in individuals with elevated leptin levels, suggesting that leptin may be an important modifier of this effect consistent with 25-OH-VitD-mediated inhibition of leptin. Leptin was highly correlated with the BMI/25-OH-VitD ratio (r = 0.80; P < 0.0001), consistent with a model in which BMI (adiposity) and 25-OH-VitD are the primary determinants of circulating leptin and PTH levels. This model may explain the failure of some studies to observe elevated PTH in vitamin D deficient adolescents and provides important insight into epidemiological studies exploring the associations of these individual biomarkers with chronic disease risk and mortality.

Topics: Adiponectin; Adult; Body Mass Index; Carotenoids; Diet; Female; Fruit; Humans; Hyperparathyroidism; Leptin; Lipids; Parathyroid Hormone; Regression Analysis; Risk Factors; Vegetables; Vitamin D; Vitamin D Deficiency

Vitamin D receptors are present in many tissues. Hypovitaminosis D is considered to be a risk factor for atherosclerosis.. This study explores the effects of vitamin D replacement on insulin sensitivity, endothelial function, inflammation, oxidative stress, and leptin in vitamin D-deficient subjects.. Twenty-three asymptomatic vitamin D-deficient subjects with 25-hydroxyvitamin D [25(OH)D] levels below 25 nmol/liter were compared with a control group that had a mean 25(OH)D level of 75 nmol/liter. The vitamin D-deficient group received 300,000 IU im monthly for 3 months. The following parameters were evaluated before and after treatment: vitamin D metabolites, leptin, endothelial function by brachial artery flow mediated dilatation (FMD), insulin sensitivity index based on oral glucose tolerance test, and lipid peroxidation as measures of thiobarbituric acid reactive substances (TBARS).. FMD measurements were significantly lower in 25(OH)D-deficient subjects than controls (P = 0.001) and improved after replacement therapy (P = 0.002). Posttreatment values of TBARS were significantly lower than pretreatment levels (P < 0.001). A positive correlation between FMD and 25(OH)D (r = 0.45; P = 0.001) and a negative correlation between FMD and TBARS (r = -0.28; P < 0.05) were observed. There was a significant increase in leptin levels after therapy, and the leptin levels were positively correlated with 25(OH)D levels (r = 0.45; P < 0.05).. This study shows that 25(OH)D deficiency is associated with endothelial dysfunction and increased lipid peroxidation. Replacement of vitamin D has favorable effects on endothelial function. Vitamin D deficiency can be seen as an independent risk factor of atherosclerosis. Hypovitaminosis D-associated endothelial dysfunction may predispose to higher rates of cardiovascular disease in the winter.

Topics: Adult; Atherosclerosis; Biomarkers; Blood Flow Velocity; Blood Pressure; Brachial Artery; Endothelium, Vascular; Female; Humans; Insulin Resistance; Leptin; Linear Models; Lipid Peroxidation; Male; Oxidative Stress; Risk Factors; Treatment Outcome; Vitamin D; Vitamin D Deficiency; Waist-Hip Ratio

Serum 25-hydroxyvitamin D (25(OH)D) is low in obese adults.. To examine serum 25(OH)D in obese (BMI >95th percentile for age) vs. non-obese (BMI = 5th-75th percentile for age) 6-10-year-old African American children and compare their differences in therapeutic response to vitamin D supplementation.. In an open label non-randomized pre-post comparison 21 obese (OB) and 20 non-obese (non-OB) subjects matched for age, sex, skin color, and pubertal maturation were treated with 400 IU of vitamin D(3) daily for 1 month. Serum 25(OH)D, 1,25-dihydroxyvitamin D (1,25(OH)(2)D), parathyroid hormone (PTH), leptin, and markers of bone turnover (serum bone-specific alkaline phosphatase (BSAP), osteocalcin (OC), and urine n -telopeptide cross-links of type 1 collagen (urine NTX)) were measured. Vitamin D deficiency was defined as serum 25(OH)D < or =20 ng/ml and insufficiency as 21-29 ng/ml respectively.. Vitamin D deficiency occurred in 12/21 (57%) OB vs. 8/20 (40%) non-OB at baseline (P = 0.35) and persisted in 5/21 (24%) OB vs. 2/18 (11%) non-OB (P = 0.42) after treatment. When the cohort was stratified by the baseline levels of 25(OH)D, there were differences in the response to treatment in the obese and non-obese cohorts.. Vitamin D deficiency was common among OB and non-OB preadolescent African American children, and 400 IU of vitamin D(3) (2x the recommended adequate intake) daily for 1 month was inadequate to raise their blood levels of 25(OH)D to > or =30 ng/ml.

Topics: Alkaline Phosphatase; Black or African American; Bone and Bones; Child; Collagen Type I; Dietary Supplements; Dose-Response Relationship, Drug; Female; Humans; Leptin; Male; Obesity; Osteocalcin; Patient Compliance; Peptides; Prevalence; Vitamin D; Vitamin D Deficiency

Vitamin D has been variably implicated in risk of developing type 1 diabetes based on cohorts of at-risk individuals. Emergent type 1 diabetes in childhood is putatively preceded by altered growth.. We explored whether polymorphisms in vitamin D metabolism genes modify risk of type 1 diabetes via effects on growth in a prospective, population-based cohort of infants.. The Cambridge Baby Growth Study enrolled newborns from Cambridgeshire, UK, for follow-up in infancy. In 612 infants, we genotyped single nucleotide polymorphisms in vitamin D metabolism genes that relate with type 1 diabetes: rs10741657 and rs12794714 in CYP2R1, rs12785878 in DHCR7, and rs10877012 in CYP27B1. Multivariate linear regression analyses tested associations between genotypes and anthropometric indices (weight, length, and skinfold thickness) or growth-related hormones (C-peptide, IGF-1, and leptin) in infancy.. Birth weight showed borderline associations with the diabetes risk-increasing alleles in CYP2R1, rs10741657 (β = -.11, P = .02) and rs12794714 (β = -.09, P = .04). The risk-increasing allele rs12794714 was also associated with higher IGF-1 levels at age 24 months (β = .30, P = .01). At age 3 months, the risk-increasing allele rs12785878 in DHCR7, known to negatively associate with 25-hydroxyvitamin D levels, showed a positive association with leptin levels (β = .23, P = .009), which was pronounced in girls (P = .004) vs boys (P = .7).. The vitamin D metabolism genes DHCR7 and CYP2R1 might influence infancy leptin and IGF-1 levels respectively. These findings open the possibility for a developmental role of vitamin D that is mediated by growth-related hormones with implications for the onset of type 1 diabetes autoimmunity.

Topics: Child, Preschool; Cholestanetriol 26-Monooxygenase; Cytochrome P450 Family 2; Diabetes Mellitus, Type 1; Female; Genetic Predisposition to Disease; Genotype; Humans; Infant; Infant, Newborn; Insulin-Like Growth Factor I; Leptin; Male; Polymorphism, Single Nucleotide; Prospective Studies; Vitamin D; Vitamin D Deficiency; Vitamins

Previous studies have been reported that vitamin D deficiency increased the risk of metabolic syndrome (MetS). Nonetheless, the exact mechanisms underlying this association is unclear. Besides, inflammation and deregulation of adipokines secretion have been recognized as pivotal factors that contribute to the pathogenesis of these conditions. Therefore, we assessed whether serum vitamin D status is associated with serum levels of adipokines and inflammatory markers in these patients.. This case-control study was carried out among 65 patients with MetS who had vitamin D insufficiency (cases) and 130 MetS patients who had vitamin D sufficiency (controls). Cases and controls were recruited from among those referred to health centers in Zabol County, Iran. Vitamin D insufficiency was regarded as a serum 25-hydroxyvitamin D [25(OH)D] concentration below 30 ng/ml. Serum concentrations of leptin, adiponectin, visfatin, and resistin and also adiponectin/leptin ratio along with serum levels of interleukin 6 (IL-6), IL-10 and tumor necrosis factor-alpha (TNF-α), were evaluated.. Serum levels of leptin, resistin, and TNF-α were significantly higher, whereas, serum adiponectin and adiponectin/leptin ratio were significantly lower in cases than the controls. There was no significant difference in serum visfatin, IL-6, and IL-10 between the groups. Serum levels of 25(OH)D were inversely correlated with leptin, resistin, and TNF-α in both unadjusted models and after adjustment for potential confounders.. Our findings indicated that vitamin D insufficiency in MetS patients is associated with increased inflammation and serum adipokine abnormalities which may be associated with developing metabolic complications in these patients.

Topics: Adipokines; Adiponectin; Case-Control Studies; Humans; Inflammation; Interleukin-10; Interleukin-6; Leptin; Metabolic Syndrome; Nicotinamide Phosphoribosyltransferase; Resistin; Tumor Necrosis Factor-alpha; Vitamin D; Vitamin D Deficiency; Vitamins

Obesity has been associated with elevated leptinemia and vitamin D deficiency. To date, whether there is an association between vitamin D and leptin levels independent from adiposity remains uncertain. Our objective was to investigate the associations between changes in 25(OH) vitamin D levels, changes in adiposity variables, and changes in leptin levels produced by a 1-year lifestyle intervention program.. Sedentary men (n = 113) with abdominal obesity, dyslipidemic, and non-vitamin D supplemented were involved in a 1-year lifestyle modification program. Subjects were individually counseled by a kinesiologist and a nutritionist once every 2 weeks during the first 4 months with subsequent monthly visits in order to elicit a 500 kcal daily energy deficit and to increase physical activity/exercise habits. Adiposity mapping by computed tomography and cardiometabolic biomarkers, as well as vitamin D measurements were performed at baseline and at the 1-year visit.. In response to a 1-year lifestyle intervention, changes in 25(OH) vitamin D levels were independently associated with changes in leptinemia after adjustment for adiposity changes. This finding supports a possible physiological link between leptinemia and 25(OH) vitamin D levels independent from adiposity and underscores the role of lifestyle modifications leading to lowered leptinemia in the clinical management of vitamin D deficiency.

Topics: Adult; Cohort Studies; Health Promotion; Humans; Hydroxycholecalciferols; Intra-Abdominal Fat; Leptin; Life Style; Male; Middle Aged; Obesity, Abdominal; Vitamin D Deficiency

Vitamin D deficiency (VDD) is common in tuberculosis (TB) and may be implicated in the etiology of the disease and in its clinical course. The aim of this study was to investigate the association between leptin, inflammatory markers and VD status in TB patients, stratified for presence or absence of diabetes mellitus (DM). Two hundred ninety-nine TB patients were recruited from October 2015 to August 2016. Also, 91 normal controls were included. The information including socio-demographics, dietary intake and living habits was obtained by face-to-face interview. Serum concentrations of leptin and TNF-α, CRP and IL-6 were compared between TB patients with and without severe VDD (SVDD). Pearson's correlation was used to analyze the association between TNF-α, leptin and 25-hydroxyvitamin D (25(OH)D). A significantly higher prevalence of VDD and SVDD was observed in TB patients compared with normal controls (93.0% vs 70.3%, 65.9% vs 3.3% respectively). Concentration of leptin was significantly lower, while TNF-α higher in TB patients with SVDD compared to those without (p<0.05). After adjustment for confounders, leptin was positively associated with 25(OH)D (r=0.210, p=0.002) with similar correlation in TB patients with DM (r=0.240, p=0.020). A negative association between TNF-α and 25(OH)D was observed (r=-0.197, p=0.003), which was significant only in the subgroup without DM (r=-0.304, p=0.001). Our findings indicate that a higher VD status in TB patients may be related to higher immune activity and less serious tissue damage, and that this relation is different according to presence or absence of DM co-morbidity.

Topics: Adolescent; Adult; Aged; C-Reactive Protein; Cross-Sectional Studies; Female; Humans; Interleukin-6; Leptin; Male; Middle Aged; Nutritional Status; Prevalence; Tuberculosis, Pulmonary; Tumor Necrosis Factor-alpha; Vitamin D; Vitamin D Deficiency; Young Adult

This study aimed to evaluate the longitudinal association of vitamin D status with glycaemia, insulin, homoeostatic model assessment of insulin resistance, adiponectin and leptin. A prospective cohort with 181 healthy, pregnant Brazilian women was followed at the 5th-13th, 20th-26th and 30th-36th gestational weeks. In this cohort, 25-hydroxyvitamin D (25(OH)D) plasma concentrations were analysed using liquid chromatography-tandem MS. Vitamin D status was categorised as sufficient or insufficient using the Endocrine Society Practice Guidelines (≥75/<75 nmol/l) and the Institute of Medicine (≥50/<50 nmol/l) thresholds. Linear mixed-effect regression models were employed to evaluate the association between vitamin D status and each outcome, considering interaction terms between vitamin D status and gestational age (P<0·1). At baseline, 70·7 % of pregnant women had 25(OH)D levels <75 nmol/l and 16 % had levels <50 nmol/l. Women with sufficient vitamin D status at baseline, using both thresholds, presented lower glycaemia than those with insufficient 25(OH)D. Pregnant women with 25(OH)D concentrations <75 nmol/l showed lower insulin (β=-0·12; 95 % CI -0·251, 0·009; P=0·069) and adiponectin (β=-0·070; 95 % CI -0·150, 0·010; P=0·085) concentrations throughout pregnancy than those with 25(OH)D levels ≥75 nmol/l. Pregnant women with 25(OH)D <50 nmol/l at baseline presented significantly higher leptin concentrations than those with 25(OH)D levels ≥50 nmol/l (β=-0·253; 95 % CI -0·044, 0·550; P=0·095). The baseline status of vitamin D influences the biomarkers involved in glucose metabolism. Vitamin D-sufficient women at baseline had higher increases in insulin and adiponectin changes throughout gestation than those who were insufficient.

Topics: Adipokines; Adiponectin; Adult; Blood Glucose; Brazil; Cohort Studies; Diabetes, Gestational; Diet; Female; Gestational Age; Humans; Insulin; Insulin Resistance; Leptin; Pregnancy; Pregnancy Complications; Prospective Studies; Vitamin D; Vitamin D Deficiency

This study aimed to evaluate the association between serum vitamin D levels and nonalcoholic fatty liver disease (NAFLD) parameters, such as metabolic syndrome (MS), inflammatory cytokines (tumor necrosis factor, high sensitive C-reactive protein) and adipokines (adiponectin, leptin).. From August 2013 to August 2016, a community-based study was performed in the north-eastern region of Taiwan. All subjects received a demographic survey, blood testing and abdominal ultrasonography (US). The vitamin D level was evaluated by quartile divide or used the classification of deficiency (< 20 ng/ml), insufficiency (20-30 ng/ml) and sufficiency (> 30 ng/ml).. Subjects were divided into NAFLD group and normal control (subjects number = 564 in each group) following abdominal US study and matching age and gender. The mean age was 57.1 years in NAFLD group and 57.5 in control group. Subjects in NAFLD group had a lower mean vitamin D than those in the control group (28.5 ± 9.5 ng/ml vs. 29.9 ± 10.2 ng/ml, P = 0.018). Subjects with serum vitamin D deficiency or insufficiency had higher odds for MS than those with sufficient vitamin D levels [deficiency vs. sufficiency, adjusted odds ratio (aOR) =1.860 (95% CI = 1.234-2.804), P = 0.003; insufficiency vs. sufficiency, aOR = 1.669 (95% CI = 1.237-2.251), P = 0.001]. Similarly, subjects in the lowest quartile of vitamin D had higher odds for MS than those in the highest quartile of vitamin D (aOR = 2.792, 95% CI = 1.719-4.538, P < 0.001). Vitamin D level was positively correlated with age and male, but negatively correlated with serum leptin level.. Subjects with low vitamin D level had higher odds for MS, but higher levels of leptin, compared to those with high vitamin D levels.

Topics: C-Reactive Protein; Female; Humans; Leptin; Male; Metabolic Syndrome; Middle Aged; Non-alcoholic Fatty Liver Disease; Taiwan; Tumor Necrosis Factor-alpha; Vitamin D Deficiency

Vitamin D is a fat soluble vitamin involved in calcium and bone metabolism; recently its deficiency has been related to cardiovascular disease. In cardiac tissue, vitamin D suppresses metalloproteinases (MMPs) expression, enzymes directly associated with vulnerable plaque.. To investigate whether the association between vitamin D and leptin is related to markers of vulnerable plaque, such as MMPs in patients with acute myocardial infarction.. We studied 66 male patients with acute myocardial infarction, undergoing primary angioplasty. Blood samples were obtained at admission and 24hs after the surgery. Leptin and vitamin D concentrations in serum and MMP-2 and -9 activities in plasma were determined.. MMP-2 activity was increased in Vitamin D deficient/insufficient patients at admission (p=0.04) and 24 hs later (p=0.05). In a linear regression model, vitamin D explained 24% of the variance of MMP-2 activity (F=2.839 p=0.04). At admission, vitamin D correlated with serum leptin (r=-0.302 p=0.033), and explained 39.5% of its variation (F=4.432 p=0.003).. In the studied population, vitamin D was inversely related to MMP-2 and leptin which are involved in coronary artery disease and acute myocardial infarction. The decrease in this hormone levels would be associated with a worse metabolic profile in acute coronary syndrome patients.

Topics: Adult; Aged; Biomarkers; Coronary Artery Disease; Humans; Leptin; Male; Matrix Metalloproteinase 2; Middle Aged; Plaque, Atherosclerotic; Rupture, Spontaneous; ST Elevation Myocardial Infarction; Time Factors; Vitamin D; Vitamin D Deficiency

Hyperandrogenic state in females is accompanied with metabolic syndrome, insulin resistance and vascular pathologies. A total of 67%-85% of hyperandrogenic women suffer also from vitamin D deficiency. We aimed to check a potential interplay between hyperandrogenism and vitamin D deficiency in producing insulin resistance and effects on coronary resistance arteries. Adolescent female rats were divided into four groups, 11-12 animals in each. Transdermal testosterone-treated and vehicle-treated animals were kept either on vitamin D-deficient or on vitamin D-supplemented diet for 8 weeks. Plasma sexual steroid, insulin, leptin and vitamin D plasma levels were measured, and oral glucose tolerance test was performed. In coronary arterioles, insulin receptor and vitamin D receptor expressions were tested by immunohistochemistry, and insulin-induced relaxation was measured in vitro on isolated coronary resistance artery segments. Testosterone impaired glucose tolerance, and it diminished insulin relaxation but did not affect the expression of insulin and vitamin D receptors in vascular tissue. Vitamin D deficiency elevated postprandial insulin levels and homeostatic model assessment insulin resistance. It also diminished insulin-induced coronary arteriole relaxation, while it raised the expression of vitamin D and insulin receptors in the endothelial and medial layers. Our conclusion is that both hyperandrogenism and vitamin D deficiency reduce sensitivity of coronary vascular tissue to insulin, but they do it with different mechanisms.

Topics: Animals; Arterioles; Biomarkers; Blood Glucose; Coronary Artery Disease; Coronary Vessels; Disease Models, Animal; Female; Glucose Tolerance Test; Gonadal Steroid Hormones; Hyperandrogenism; Insulin; Insulin Resistance; Leptin; Polycystic Ovary Syndrome; Rats, Wistar; Time Factors; Vascular Resistance; Vasodilation; Vitamin D; Vitamin D Deficiency

Topics: Adiponectin; Adult; Body Mass Index; Cross-Sectional Studies; Female; Gene Expression; Humans; Leptin; Male; Middle Aged; Obesity, Abdominal; Prevalence; Russia; Vitamin D; Vitamin D Deficiency; Waist Circumference

Metabolic syndrome (MetS) is more common in HIV-infected adults and children than in the general population. Adipocytokines and inflammatory markers may contribute to the pathophysiology of this condition and could be useful indices for monitoring MetS. The objective of this study was to provide information on the prevalence of MetS and investigate the role of adipocytokines and other biomarkers in this syndrome in HIV-infected pediatric patients.. A cross-sectional study was conducted between October 2013 and March 2014 in the outpatient clinics of 2 tertiary pediatric referral hospitals. Fifty-four HIV-infected children and adolescents were included. MetS was defined according to the International Diabetes Federation and modified National Cholesterol Education Program Adult Treatment Panel III criteria. Measurements included anthropometry, waist circumference, blood pressure, fasting lipids, glucose and insulin, adiponectin, leptin, interleukin-6, vitamin D and C-reactive protein and clinical lipodystrophy assessment.. Among the total, 3.7% of patients met the International Diabetes Federation criteria for MetS and 7.4% met the National Cholesterol Education Program Adult Treatment Panel III criteria. C-reactive protein and leptin levels were significantly higher and adiponectin level significantly lower in patients with MetS, regardless of the criteria used. Insulin resistance was observed in 40.7% of patients; abnormal quantitative insulin sensitivity check index values were found in 88.9%. Eighteen patients (33.3%) had vitamin D deficiency.. The prevalence of MetS was similar to that observed in larger cohorts of HIV-infected patients in our setting. Adipocytokine dysregulation seems to be related to MetS in HIV-infected children. A high percentage of patients showed insulin resistance, which should be strictly monitored.

Topics: Adiponectin; Adolescent; Biomarkers; Child; Cross-Sectional Studies; Female; HIV-Associated Lipodystrophy Syndrome; Humans; Insulin Resistance; Leptin; Male; Metabolic Syndrome; Risk Factors; Spain; Vitamin D Deficiency

To investigate the impact of vitamin D deficiency on insulin resistance and abnormal glucose homeostasis in obesity.. Sixty male C57BL/6 mice (3 months old) were fed a control diet (C-10% energy as fat) or a high-fat diet (HF-50% energy as fat), with or without vitamin D, for 8 weeks. There was no difference in body mass between the HF and HF/VitD- groups. Vitamin D deficiency (VitD) in the diet-induced obese mice increased hyperinsulinemia (p = 0.04), hyperleptinemia (p = 0.0002), insulin resistance (HOMA-IR, p = 0.04), and islet changes, including alpha and beta cell disarray. In the insulin signaling pathway, insulin receptor substrate 2 expression was upregulated in the C/VitD- group (p = 0.001) and downregulated in the HF/VitD- group (p = 0.009). Interestingly, forkhead box protein O1 expression was higher in the HF/VitD- group than in the HF group (p = 0.03), and pancreatic and duodenal homeobox 1 expression was lower in the HF/VitD-group than in the HF group (p = 0.025), indicating that the HF diet and vitamin D deficiency influenced the downregulation of the expression of these proteins (two-way ANOVA, p < 0.0001).. Vitamin D deficiency exacerbated the adverse structural and physiological remodeling of pancreatic islets due to obesity, contributing to abnormal glucose homeostasis.

Topics: Adiponectin; Animals; Body Weight; Carbohydrate Metabolism; Diet, High-Fat; Insulin; Islets of Langerhans; Leptin; Male; Mice, Inbred C57BL; Obesity; Phosphatidylinositol 3-Kinases; Proto-Oncogene Proteins c-akt; Signal Transduction; Vitamin D Deficiency

The associations between Helicobacter pylori infection, serum vitamin D level, and metabolic syndrome (MS) are controversial. The present community-based study aimed to investigate the effect of H pylori infection and serum vitamin D deficiency on MS development.Individuals from the northeastern region of Taiwan were enrolled in a community-based study from March, 2014 to August, 2015. All participants completed a demographic survey and underwent the urea breath test (UBT) to detect H pylori infection as well as blood tests to determine levels of vitamin D, adiponectin, leptin, and high-sensitivity C-reactive protein. The ATP III criteria for MS were used in this study.A total of 792 men and 1321 women were enrolled. The mean age was 56.4 ± 13.0 years. After adjusting for age and sex, the estimated odds of MS development for a UBT-positive subject were 1.503 (95% confidence interval [CI]: 1.206-1.872, P < 0.001) when compared to a UBT-negative subject. For participants with vitamin D deficiency (<20 ng/mL), the odds of MS development were 1.423 (95% CI: 1.029-1.967, P = 0.033) when compared to those with sufficient vitamin D level (>30 ng/mL). For participants with both H pylori infection and vitamin D deficiency, the odds of MS development were 2.140 (95% CI: 1.348-3.398, P = 0.001) when compared to subjects without H pylori infection and with sufficient vitamin D levels.H pylori infection and vitamin D deficiency could be predictors of MS. For individuals with both H pylori infection and vitamin D deficiency, the odds of MS development were 2.140 when compared to individuals without H pylori infection and with sufficient vitamin D levels.

Topics: Adiponectin; Adult; Aged; Breath Tests; C-Reactive Protein; Female; Helicobacter Infections; Helicobacter pylori; Humans; Leptin; Male; Metabolic Syndrome; Middle Aged; Taiwan; Urea; Vitamin D; Vitamin D Deficiency

Vitamin D deficiency and dysfunctional adipose tissue are involved in the development of cardiometabolic disturbances (eg, hypertension, insulin resistance, type 2 diabetes mellitus, obesity, and dyslipidemia). We evaluated the relation between vitamin D and adipocytokines derived from adipose tissue. We studied 50 obese individuals who were classified into different subgroups according to medians of observed anthropometric parameters (body mass index, body fat percentage, waist circumference, and trunk fat mass). There was a negative correlation between vitamin D level and leptin and resistin (r = -.61, P < .01), while a positive association with adiponectin concentrations was found (r = .7, P < .001). Trend estimation showed that increase in vitamin D level is accompanied by intensive increase in adiponectin concentrations (growth coefficient: 12.13). In conclusion, a positive trend was established between vitamin D and the protective adipocytokine adiponectin. The clinical relevance of this relationship needs to be investigated in larger studies.

Topics: Adiponectin; Adipose Tissue; Adult; Anthropometry; Biomarkers; Enzyme-Linked Immunosorbent Assay; Female; Humans; Immunoenzyme Techniques; Leptin; Male; Obesity; Resistin; Vitamin D; Vitamin D Deficiency

Millions of Mexico, US and across the world children are overweight and obese. Exposure to fossil-fuel combustion sources increases the risk for obesity and diabetes, while long-term exposure to fine particulate matter (PM2.5) and ozone (O3) above US EPA standards is associated with increased risk of Alzheimer's disease (AD). Mexico City Metropolitan Area children are chronically exposed to PM2.5 and O3 concentrations above the standards and exhibit systemic, brain and intrathecal inflammation, cognitive deficits, and Alzheimer disease neuropathology. We investigated adipokines, food reward hormones, endothelial dysfunction, vitamin D and apolipoprotein E (APOE) relationships in 80 healthy, normal weight 11.1±3.2 year olds matched by age, gender, BMI and SES, low (n: 26) versus high (n:54) PM2.5 exposures. Mexico City children had higher leptin and endothelin-1 (p<0.01 and p<0.000), and decreases in glucagon-like peptide-1 (GLP 1), ghrelin, and glucagon (<0.02) versus controls. BMI and leptin relationships were significantly different in low versus high PM2.5 exposed children. Mexico City APOE 4 versus 3 children had higher glucose (p=0.009). Serum 25-hydroxyvitamin D<30 ng/mL was documented in 87% of Mexico City children. Leptin is strongly positively associated to PM 2.5 cumulative exposures. Residing in a high PM2.5 and O3 environment is associated with 12h fasting hyperleptinemia, altered appetite-regulating peptides, vitamin D deficiency, and increases in ET-1 in clinically healthy children. These changes could signal the future trajectory of urban children towards the development of insulin resistance, obesity, type II diabetes, premature cardiovascular disease, addiction-like behavior, cognitive impairment and Alzheimer's disease. Increased efforts should be made to decrease pediatric PM2.5 exposures, to deliver health interventions prior to the development of obesity and to identify and mitigate environmental factors influencing obesity and Alzheimer disease.

Topics: Adolescent; Alzheimer Disease; Body Weight; Case-Control Studies; Child; Cohort Studies; Endothelin-1; Hormones; Humans; Leptin; Mexico; Obesity; Particulate Matter; Vitamin D Deficiency

Vitamin D deficiency and metabolic syndrome are 2 very common health problems in the Spanish population. It has been suggested that patients with metabolic syndrome may be vitamin D deficient more often than subjects without it and that low vitamin D levels may predispose to metabolic syndrome development. However, the results of prospective and intervention studies have been different and such relationship remains unclear. We assessed the relationship between 25-hydroxyvitamin D levels and the prevalence and incidence of metabolic syndrome.. We undertook a population-based cohort study in Spain. At baseline (1996-1998), 1,226 subjects were evaluated. Follow-up visits were performed in 2002-2004 and 2005-2007.At baseline and follow-up, participants underwent an interview and a standardized clinical examination with an oral glucose tolerance test in those subjects without known diabetes. At the second visit, 25-hydroxyvitamin D levels and intact parathyroid hormone levels were measured.. The prevalence of metabolic syndrome at the second and third visit was 29.4 and 42.5%, respectively. Mean levels of 25-hydroxyvitamin D were lower in subjects with metabolic syndrome: 21.7 (6.21) vs 23.35 (6.29) ng/ml, P<.001.The prevalence of vitamin D deficiency (25-hydroxyvitamin D<20 ng/ml) at the second evaluation was 34.7%, with significant differences between subjects with and without metabolic syndrome(34.6 vs 26.5%, P<.01). Men with vitamin D deficiency had more frequently hypertension and metabolic syndrome than men with normal levels. Women with vitamin D deficiency had more frequently hyperglycemia, hypertension, increased waist circumference and hypertriglyceridemia. In a prospective study, 25-hydroxyvitamin D values<20 ng/ml were not significantly associated with an increased risk of developing metabolic syndrome in the next 5 years (odds ratio 0,99, 95% confidence interval 0.57-1.7, P=.97) after adjusting by sex and age.. Vitamin D deficiency is associated with an increased prevalence but not with an increased incidence of metabolic syndrome.

Topics: Adiponectin; Adult; Body Mass Index; Comorbidity; Female; Follow-Up Studies; Glucose Tolerance Test; Humans; Hypertension; Hypertriglyceridemia; Interleukin-6; Leptin; Lipids; Male; Metabolic Syndrome; Middle Aged; Prevalence; Prospective Studies; Resistin; Risk Factors; Sex Factors; Tumor Necrosis Factor-alpha; Vitamin D; Vitamin D Deficiency; Waist Circumference

Psoriasis is a disorder caused by genetic and immunological factors. Leptin, a peptide hormone secreted predominantly from adipose tissue, regulates energy intake and expenditure, as well as the T-helper response. There have been conflicting reports regarding serum levels of leptin and adiponectin in patients with psoriasis. In the present study, we measured serum levels of leptin and adiponectin in Korean patients with psoriasis. Twenty-four patients with psoriasis and fifteen control subjects were included in the study. Serum leptin and adiponectin levels were determined by an immunometric sandwich enzyme-linked immunosorbent assay (ELISA). The mean serum leptin concentration in patients with psoriasis was higher than in controls, and the difference was statistically significant. In contrast, serum adiponectin levels in patients with psoriasis were significantly decreased compared with healthy controls. Leptin levels in vitamin D-deficient patients were statistically significantly higher than in vitamin D-sufficient patients. Serum adiponectin concentrations showed a negative correlation with body mass index (BMI) and psoriasis area and severity index (PASI) in patients with psoriasis. In conclusion, the present study demonstrated that leptin and adiponectin may play a role in the immunopathogenesis of psoriasis and may be useful biomarkers indicating severity of psoriasis in Korean patients.

Topics: Adiponectin; Adult; Aged; Biomarkers; Body Mass Index; Enzyme-Linked Immunosorbent Assay; Female; Humans; Inflammation; Leptin; Male; Middle Aged; Psoriasis; Republic of Korea; Risk; Severity of Illness Index; Vitamin D; Vitamin D Deficiency; Young Adult

The vitamin D endocrine system is functional in the adipose tissue, as demonstrated in vitro, in cultured adipocytes, and in vivo in mutant mice that developed altered lipid metabolism and fat storage in the absence of either 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] or the vitamin D receptor. The aim of the present study was to examine the role of vitamin D and calcium on body adiposity in a diet-induced vitamin D deficient rat model. Vitamin D-deficient rats gained less weight and had lower amounts of visceral fat. Consistent with reduced adipose tissue mass, the vitamin D-deficient rats had low circulating levels of leptin, which reflects body fat stores. Expression of vitamin D and calcium sensing receptors, and that of genes involved in adipogenesis such as peroxisome proliferator-activated receptor, fatty acid synthase and leptin were significantly reduced in white adipose tissue of deficient rats compared to vitamin D-sufficient rats. Furthermore, the expression of uncoupling proteins (Ucp1 and Ucp2) was elevated in the white adipose tissue of the deficient rat indicative of higher energy expenditure, thereby leading to a lean phenotype. Expression of the p160 steroid receptor coactivator3 (SRC3), a key regulator of adipogenesis in white adipose tissue was decreased in vitamin D-deficient state. Interestingly, most of the changes observed in vitamin D deficient rats were corrected by calcium supplementation alone. Our data demonstrates that dietary vitamin D and calcium regulate adipose tissue function and metabolism.

Topics: Adipogenesis; Adiponectin; Adipose Tissue; Adiposity; Animals; Calcium; Diet; Fatty Acid Synthase, Type I; Gene Expression; Hypocalcemia; Insulin; Ion Channels; Leptin; Lipids; Liver; Male; Mitochondrial Proteins; Nuclear Receptor Coactivator 3; PPAR gamma; Rats, Sprague-Dawley; Uncoupling Protein 1; Uncoupling Protein 2; Vitamin D Deficiency

The aim of the study was to estimate potential associations of vitamin D concentration with metabolic and hormonal indices in women with polycystic ovary syndrome (PCOS) presenting abdominal and gynoidal type of obesity.. Twenty-six women with PCOS (19-49 years old, BMI: 26.8-53.8 kg/m2), presenting predominantly abdominal and gynoidal type of obesity were recruited. Anthropometric measures, body composition using dual-energy absorptiometry, fasting serum 25-hydroxyvitamin D, leptin, glucose, insulin, homeostatic model of assessment (HOMA), lipids, androgens and sex hormone-binding globulin (SHGB) were estimated.. Vitamin D insufficiency was found in 2, and deficiency or deep deficiency in 12 patients. Levels of vitamin D were lower in obese than non-obese women, and in patients with abdominal as compared to gynoidal obesity (9.60±3.7 vs. 16.02±3.3 ng/mL, p<0.04). In obese women, vitamin D correlated negatively with all, except for gynoidal fat, measures of obesity fasting glucose levels, and HOMA. No correlations with androgens were found. In women with abdominal obesity vitamin D correlated with luteinizing hormone/follicle-stimulating hormone ratio (LH/FSH) and SHBG.. We demonstrated that women with PCOS are often vitamin D deficient. Its concentration was lower in patients with predominantly abdominal obesity as compared to subjects with gynoidal fat excess. In overweight/obese subjects with PCOS, vitamin D correlated with fasting glucose and HOMA. The correlation with LH/FSH suggests that vitamin D status may contribute to hormonal dysregulation. Further studies are needed to elucidate a potentially different impact of abdominal and subcutaneous fat on vitamin D metabolism.

Topics: Adult; Androgens; Blood Glucose; Female; Humans; Leptin; Metabolic Syndrome; Middle Aged; Polycystic Ovary Syndrome; Sex Hormone-Binding Globulin; Vitamin D; Vitamin D Deficiency; Young Adult

Infants are at risk of vitamin D insufficiency, owing to their limited exposure to direct sunlight and the low levels of vitamin D in breast milk. Although vitamin D insufficiency has been associated with cardiometabolic risk factors in children, these associations have not been studied in infants, despite their unique risks. Therefore, we sought to determine whether vitamin D status was associated with cardiometabolic measures in infants.. Ninety-nine full-term infants were evaluated at the age of 1 y with measurement of 25-hydroxy vitamin D (25-OH-D) and an array of traditional (fasting glucose, insulin, low-density-lipoprotein cholesterol, high-density-lipoprotein cholesterol, triglycerides) and emerging (C-reactive protein, adiponectin, leptin) cardiometabolic risk factors. On the basis of 25-OH-D levels, infants were classified as vitamin D sufficient (n = 59), vitamin D insufficient (n = 29), or vitamin D deficient (n = 11).. Duration of exclusive breastfeeding and prevalence of nonwhite ethnicity were highest in the vitamin D-deficient group (P = 0.05 and 0.03, respectively). Current use of vitamin D supplementation was highest in the sufficient group (P = 0.02). Of note, however, there were no significant differences among the three groups in any of the cardiometabolic risk factors, on both unadjusted and covariate-adjusted analyses.. Vitamin D insufficiency/deficiency is not associated with an adverse cardiometabolic risk factor profile in 1-y-old infants.

Topics: Adiponectin; Biomarkers; Breast Feeding; C-Reactive Protein; Cardiovascular Diseases; Cholesterol; Enzyme-Linked Immunosorbent Assay; Humans; Infant; Insulin; Leptin; Luminescent Measurements; Metabolic Diseases; Radioimmunoassay; Risk Factors; Statistics, Nonparametric; Triglycerides; Vitamin D Deficiency

Evidence for a role of vitamin D in maintaining normal glucose homeostasis is inconclusive. We sought to clarify the relationship between maternal and fetal insulin resistance and vitamin D status. This is a prospective cohort study of 60 caucasian pregnant women. Concentrations of 25-hydroxyvitamin D (25-OHD), glucose, insulin, and leptin were measured in early pregnancy and at 28 weeks. Ultrasound at 34 weeks assessed fetal anthropometry including abdominal wall width, a marker of fetal adiposity. At delivery birth weight was recorded and fetal 25-OHD, glucose, C-peptide, and leptin measured in cord blood. Insulin resistance was calculated using the Homeostasis Model Assessment (HOMA) equation. We found that those with lower 25-OHD in early pregnancy had higher HOMA indices at 28 weeks, (r = -.32, P = .02). No significant relationship existed between maternal or fetal leptin and 25-OHD, or between maternal or fetal 25-OHD and fetal anthropometry or birth weight. The incidence of vitamin D deficiency was high at each time point (15%-45%). These findings lend support to routine antenatal supplementation with vitamin D in at risk populations.

Topics: Adiposity; Biomarkers; Blood Glucose; Female; Fetal Blood; Fetal Development; Fetal Macrosomia; Gestational Age; Homeostasis; Humans; Insulin; Insulin Resistance; Leptin; Longitudinal Studies; Pregnancy; Prospective Studies; Risk Factors; Vitamin D; Vitamin D Deficiency

Associations between 25 hydroxy vitamin D [25(OH)D], adipokines levels, and insulin resistance have been reported. The aim of this study was to explore the effects of cholecalciferol supplementation on vitamin D levels, insulin resistance, leptin, and adiponectin levels in vitamin D-deficient peritoneal dialysis (PD) patients.. In nineteen vitamin D-deficient PD patients, who were treated with cholecalciferol, fasting serum glucose, insulin, adiponectin, leptin, 25(OH)D and parathyroid hormone (PTH) were measured before and after cholecalciferol replacement therapy. Eighteen (94.7 %) PD patients with vitamin D deficiency were receiving active vitamin D compounds (alphacalciferol) for PTH control. Alphacalciferol dosing was kept constant during treatment with cholecalciferol.. While mean 25(OH)D significantly increased from (10.2 ± 4.9 ng/ml) to (82.9 ± 56.5 ng/ml) (p < 0.05), mean homeostatic model assessment-insulin resistance index significantly decreased from (4.6 ± 3.6) to (2.8 ± 2.0) after cholecalciferol replacement therapy (p < 0.05). Serum leptin levels (12.9 ± 17.6 ng/ml) significantly increased (18.1 ± 19.5 ng/ml) (p < 0.05), while there was no change in serum adiponectin, calcium, and phosphate after vitamin D replacement. Serum PTH levels significantly decreased from 551.9 ± 276.6 pg/ml to 434.0 ± 273.4 ng/ml.. Cholecalciferol replacement therapy significantly decreases PTH levels and insulin resistance. The results of this study need to be confirmed in larger clinical trials.

Topics: Adipokines; Cholecalciferol; Female; Follow-Up Studies; Humans; Insulin Resistance; Kidney Failure, Chronic; Leptin; Male; Middle Aged; Peritoneal Dialysis; Pilot Projects; Prospective Studies; Vitamin D; Vitamin D Deficiency; Vitamins

The study aim determined if low 25-hydroxy vitamin D levels correlated with low levels of adiponectin and insulin resistance in African American adolescents with body mass index > or = 85th %.. Fasting blood levels of adiponectin, 25-hydroxy vitamin D, insulin, glucose, lipid, leptin and glycosylated hemoglobin were measured in a total of 34 (19 study and 15 control) African American adolescents between the ages of 10 and 20 years. Nutritional vitamin D intake and body composition measurements were assessed. Insulin resistance was calculated using the homeostasis model assessment.. Adiponectin, fasting insulin, glucose, leptin, triglycerides, HDL, and 25-hydroxy vitamin D levels all reached statistical significance in the group with body mass index > or = 85th percentile when compared to the control population. There was no difference in vitamin D intake between the two groups.. Low vitamin D levels correlated with low adiponectin levels and obesity and insulin resistance.

Topics: Adiponectin; Adolescent; Adult; Black or African American; Case-Control Studies; Child; Female; Humans; Ideal Body Weight; Insulin; Insulin Resistance; Leptin; Male; Nutritional Status; Obesity; Overweight; Vitamin D; Vitamin D Deficiency; Young Adult

This cross-sectional study examined bone mineral density, bone turnover, body composition and calciotropic hormones in 24 boys with Duchenne muscular dystrophy (DMD) (2.3-19.7 years), most of whom were being treated with prednisolone, and 24 age-matched healthy boys. Our study demonstrated lower bone mineral density in the DMD group for total body, spine, hip, heel and forearm measurements. These differences between DMD patients and controls increased with increasing age. Biochemical markers of both bone formation and resorption revealed reduced bone turnover in DMD patients. The fracture rate was not higher in DMD patients. The DMD group had low vitamin D levels but high leptin levels in comparison with the control group. Muscle strength correlated with bone mineral density assessed at the hip and heel in the DMD group. Interventions that increase bone formation should be considered, as DMD patients have reduced bone turnover in addition to their low bone mineral density.

Topics: Adolescent; Adult; Biomarkers; Bone and Bones; Bone Density; Bone Resorption; Calcium; Child; Child, Preschool; Cross-Sectional Studies; Diet; Glucocorticoids; Humans; Leptin; Male; Muscle Strength; Muscular Dystrophy, Duchenne; Nutrition Assessment; Nutritional Physiological Phenomena; Osteogenesis; Osteoporosis; Prednisolone; Vitamin D Deficiency