cholecalciferol and Metabolic-Syndrome

In the last decade, an increasing awareness was directed to the role of Vitamin D in non-skeletal and preventive roles for chronic diseases. Vitamin D is an essential hormone in regulating calcium/phosphorous balance and in the pathogenesis of inflammation, insulin resistance, and obesity. The main forms of vitamin D, Cholecalciferol (Vitamin D3) and Ergocalciferol (Vitamin D2) are converted into the active form (1,25-dihydroxyvitamin D) thanks to two hydroxylations in the liver, kidney, pancreas, and immune cells. Some anti-inflammatory cytokines are produced at higher levels by vitamin D, while some pro-inflammatory cytokines are released at lower levels. Toll-Like Receptor (TLR) expression is increased, and a pro-inflammatory state is also linked to low levels of vitamin D. Regardless of how it affects inflammation, various pathways suggest that vitamin D directly improves insulin sensitivity and secretion. The level of vitamin D in the body may change the ratio of pro- to anti-inflammatory cytokines, which would impact insulin action, lipid metabolism, and the development and function of adipose tissue. Many studies have demonstrated an inverse relationship between vitamin D concentrations and pro-inflammatory markers, insulin resistance, glucose intolerance, metabolic syndrome, obesity, and cardiovascular disease. It is interesting to note that several long-term studies also revealed an inverse correlation between vitamin D levels and the occurrence of diabetes mellitus. Vitamin D supplementation in people has controversial effects. While some studies demonstrated improvements in insulin sensitivity, glucose, and lipid metabolism, others revealed no significant effect on glycemic homeostasis and inflammation. This review aims to provide insight into the molecular basis of the relationship between vitamin D, insulin resistance, metabolic syndrome, type 1 and 2 diabetes, gestational diabetes, and cardiovascular diseases.

Topics: Anti-Inflammatory Agents; Cardiovascular Diseases; Cholecalciferol; Cytokines; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Female; Humans; Inflammation; Insulin; Insulin Resistance; Metabolic Syndrome; Obesity; Pregnancy; Vitamin D; Vitamin D Deficiency; Vitamins

Vitamin D is obtained from cutaneous production when 7-dehydrocholesterol is converted to vitamin D(3) (cholecalciferol) by ultraviolet B radiation or by oral intake of vitamin D. Rickets appeared to have been conquered with vitamin D intake, and many health care professionals thought the major health problems resulting from vitamin D deficiency had been resolved. However, rickets can be considered the tip of the vitamin D deficiency iceberg. In fact, vitamin D deficiency remains common in children and adults. An individual's vitamin D status is best evaluated by measuring the circulating 25-hydroxyvitamin D (25(OH)D3) concentration. There is increasing agreement that the optimal circulating 25(OH)D3 level should be approximately 30 ng/mL or above. Using this definition, it has been estimated that approximately three-quarters of all adults have low levels. In utero and during childhood, vitamin D deficiency can cause growth retardation and skeletal deformities and may increase the risk of hip fracture later in life. Vitamin D deficiency in adults can exacerbate osteopenia and osteoporosis, cause osteomalacia and muscle weakness, and increase the risk of fracture. More recently, associations between low vitamin D status and increased risk for various non-skeletal morbidities have been recognized; whether all of these associations are causally related to low vitamin D status remains to be determined. The discovery that most tissues and cells in the body have vitamin D receptors and that several possess the enzymatic machinery to convert the 25-hydroxyvitamin D3, to the active form, 1,25-dihydroxyvitamin D3, has provided new insights into the function of this vitamin. Of great interest is its role in decreasing the risk of many chronic illnesses, including common cancers, autoimmune diseases, infectious diseases, and cardiovascular disease. In this review I consider the nature of vitamin D deficiency, discuss its role in skeletal and non-skeletal health, and suggest strategies for prevention and treatment.

Topics: Asthma; Biomarkers; Bone Density Conservation Agents; Bone Diseases, Metabolic; Cholecalciferol; Dietary Supplements; Ergocalciferols; Humans; Metabolic Syndrome; Nervous System Diseases; Parathyroid Hormone; Rickets; Risk Factors; Sunlight; Vitamin D; Vitamin D Deficiency

Both altered GH-IGF-I axis and low serum levels of 25-hydroxyvitamin D (25(OH)D) are linked to measures of metabolic syndrome. Our hypothesis was that there is a relation between GH, IGF-I, and 25(OH)D; and that vitamin D supplementation may have an effect on the levels of GH, IGF-I, and IGF-I/IGFBP-3 ratio. 318 overweight and obese subjects completed a one-year randomized intervention with either 40,000 or 20,000 IU cholecalciferol per week or placebo. GH, IGF-I, IGFBP-3 and measures of insulin resistance were evaluated at baseline and at the end of study. There was a significant relation between entities of GH-IGF-I axis and insulin resistance. Subjects with severe obesity had significantly lower serum 25(OH)D and had a significant linear decline in IGF-I/IGFBP-3 ratio with increasing serum 25(OH)D quartiles. Vitamin D status was an independent predictor of GH-IGF-I axis and supplementation with vitamin D decreased IGF-I/IGFBP-3 ratio in subjects without severe obesity. No corresponding effect of vitamin D supplementation on BMI or insulin resistance was observed. Adverse effects of GH-IGF-I axis on glucose metabolism and the development of metabolic syndrome may be in part associated with the changes in vitamin D status.

Topics: Adult; Aged; Cholecalciferol; Dietary Supplements; Dose-Response Relationship, Drug; Female; Follow-Up Studies; Glucose; Growth Hormone; Humans; Insulin Resistance; Insulin-Like Growth Factor Binding Protein 3; Insulin-Like Growth Factor I; Male; Metabolic Syndrome; Middle Aged; Obesity; Overweight; Signal Transduction

Metabolic syndrome poses additional risk for postmenopausal women who are already at risk for osteoporosis. We hypothesized that a nutritional supplement containing anti-inflammatory phytochemicals and essential bone nutrients would produce a favorable bone biomarker profile in postmenopausal women with metabolic syndrome. In this 14-week, randomized trial, 51 women were instructed to consume a modified Mediterranean-style, low-glycemic-load diet and to engage in aerobic exercise. Those in the intervention arm (n = 25) additionally received 200 mg hop rho iso-alpha acids, 100 mg berberine sulfate trihydrate, 500 IU vitamin D₃, and 500 μg vitamin K₁ twice daily. Forty-five women completed the study. Baseline nutrient intake did not differ between arms. Compared with baseline, the intervention arm exhibited an approximate 25% mean decrease (P < .001) in serum osteocalcin (indicative of bone turnover), whereas the placebo arm exhibited a 21% increase (P = .003). Serum 25-hydroxyvitamin D increased 23% (P = .001) in the intervention arm and decreased 12% (P = .03) in the placebo arm. The between-arm differences for osteocalcin and 25-hydroxyvitamin D were statistically significant. Serum insulin-like growth factor I was statistically increased in both arms, but the between-arm differences were not statistically significant. Subanalysis showed that among those in the highest tertile of baseline insulin-like growth factor I, the intervention arm exhibited a significant increase in amino-terminal propeptide of type I collagen, whereas the placebo arm showed a significant decrease at 14 weeks. Treatment with rho iso-alpha acids, berberine, vitamin D₃, and vitamin K₁ produced a more favorable bone biomarker profile indicative of healthy bone metabolism in postmenopausal women with metabolic syndrome.

Topics: Anti-Inflammatory Agents; Berberine; Biomarkers; Bone and Bones; Cholecalciferol; Collagen Type I; Dietary Supplements; Female; Humans; Humulus; Insulin-Like Growth Factor I; Metabolic Syndrome; Middle Aged; Osteocalcin; Osteoporosis, Postmenopausal; Phytotherapy; Plant Extracts; Single-Blind Method; Vitamin D; Vitamin K 1; Vitamins

Topics: Aged; Aged, 80 and over; Aging; Calcium; Cholecalciferol; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Fractures, Spontaneous; Glucose Intolerance; Humans; Male; Metabolic Syndrome; Osteoporosis; Placebos; Risk Factors; Vitamin D Deficiency; Vitamins

Vitamin D deficiency has been observed in individuals with metabolic syndrome (MetS). This study evaluated the effects of vitamin D supplementation in patients with MetS and vitamin D deficiency.. The 20-week intervention resulted in an increment of 14.3 ng/mL of 25(OH)D. HbA1c showed a reduction of 0.69% (95% CI [-1.16, -0.21], p = 0.005); however, the triglycerides, HDL-cholesterol, fasting blood glucose, blood pressure, and waist circumference were not responsive to supplementation.. Vitamin D

Topics: Cholecalciferol; Dietary Supplements; Humans; Metabolic Syndrome; Pilot Projects; Vitamin D; Vitamin D Deficiency

Metabolic syndrome (MetS) is a cluster of cardiovascular risk factors including central obesity, hypertension, insulin resistance, dyslipidemia, and hyperglyemia. MetS is found to be a positive predictor of cardiovascular morbidity and mortality. The present study was planned to test the efficacy of vitamin D3 supplementation as compared with cortisol inhibition on MetS parameters. Wistar rats were allocated into four groups: control, untreated MetS, and MetS treated with either vitamin D3 (10 µg/kg) or carbenoxolone (50 mg/kg). MetS was induced by combination of high-fat diet and oral fructose. After the induction period (8 weeks), MetS was confirmed, and treatment modalities started for a further 4 weeks. Compared with untreated MetS, vitamin D3- and carbenoxolone-treated rats showed significant reduction in blood pressure, body mass index, Lee index, waist circumference, retroperitoneal fat, and improvement of dyslipidemia. Meanwhile, treatment with carbenoxolone significantly lowered the elevated liver enzymes, and vitamin D3 resulted in improved insulin sensitivity, enhanced glucose uptake by muscles, and replenished glycogen content in the liver and muscles near control levels. In conclusion, although treatment with vitamin D3 or carbenoxolone reduced the risk factors associated with MetS, vitamin D3 was effective in ameliorating insulin resistance which is the hallmark of MetS.

Topics: Animals; Blood Glucose; Carbenoxolone; Cholecalciferol; Insulin Resistance; Metabolic Syndrome; Rats; Rats, Wistar

The current study was conducted to investigate the nephroprotective effects of vildagliptin-metformin combination in an experimental model of fructose/salt-induced metabolic syndrome (MetS). A major aim was to evaluate the potential capacity of vitamin D3 to potentiate the pleiotropic nephroprotective effects of vildagliptin-metformin combination. MetS was induced in adult male Wistar rats by adding fructose (10%) to everyday drinking water and salt (3%) to the diet for 6 weeks. Along with the same concentrations of fructose/salt feeding, MetS rats were then treated orally with either vildagliptin (10 mg/kg/day)-metformin (200 mg/kg/day) combination, vitamin D3 (10 μg/kg/day), or the triple therapy for a further 6 weeks. The incidence of MetS was confirmed 6 weeks after fructose/salt consumption, when the rats exhibited significant weight gain, dyslipidemia, hyperuricemia, insulin resistance, hyperinsulinemia, and impaired glucose tolerance. At the end of the 12-week experimental period, MetS rats displayed significantly deteriorated renal function, enhanced intrarenal oxidative stress and inflammation together with exaggerated renal histopathological damages and interstitial fibrosis. The study has corroborated antioxidant, anti-inflammatory, and antifibrotic effects of vildagliptin-metformin combination, vitamin D3, and the triple collaborative therapy, conferring renoprotection in the setting of MetS. Due attention has been paid to the crucial role of dipeptidyl peptidase-4 inhibition and sirtuin-1/5' adenosine monophosphate-activated protein kinase activation as novel therapeutic targets to optimize renoprotection. The apparent potentiating effect, evoked upon coadministration of vitamin D3 with vildagliptin-metformin combination, may provide a cornerstone for further clinical investigations.

Topics: Adamantane; Animals; Cholecalciferol; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Drug Therapy, Combination; Hypoglycemic Agents; Male; Metabolic Syndrome; Metformin; Nitriles; Pyrrolidines; Rats; Rats, Wistar; Vildagliptin

The study aimed to investigate the potential nephroprotective effects of vitamin D3 in metabolic syndrome (MetS) and the molecular basis of the underlying mechanisms of its action.. MetS was induced in adult male Wistar rat‏s by adding fructose (10%) to every day drinking water and salt (3%) to the diet. Six weeks after fructose/salt consumption, fasting serum lipid profile and uric acid levels were determined, an oral glucose tolerance test (OGTT) was performed and kidney function was checked. MetS rats were then treated orally with vitamin D3 (10 µg/kg/day) for 6 weeks. At the end of the study period (12 weeks), the OGTT test was reperformed, anthropometrical parameters were measured, urine, blood and tissue samples were collected and the animals were euthanised.. The incidence of MetS was confirmed 6 weeks after fructose/salt consumption, when the rats exhibited significant weight gain, dyslipidemia, hyperuricemia, insulin resistance, hyperinsulinemia and impaired glucose tolerance. After 12 weeks, MetS rats displayed markedly declined renal function alongside with extravagant renal histopathological damages and interstitial fibrosis. Furthermore, significantly enhanced renal oxidative stress and inflammation were manifested. Vitamin D3 supplementation in MetS rats significantly reversed all the above-mentioned deleterious effects.. The study has indeed provided mounting evidence of the promising therapeutic potential of vitamin D3 against development and progression of MetS-induced nephropathy. A new insight has been introduced into the crucial role of dipeptidyl peptidase-4 inhibition and sirtuin-1/5'adenosine monophosphate-activated protein kinase activation in the renoprotective effects of vitamin D3.

Topics: Animals; Blood Glucose; Cholecalciferol; Dietary Supplements; Fructose; Insulin Resistance; Male; Metabolic Syndrome; Rats; Rats, Wistar

Topics: Cholecalciferol; COVID-19; Female; Humans; Metabolic Syndrome; Non-alcoholic Fatty Liver Disease; Pandemics; SARS-CoV-2; Vitamin D; Vitamin D Deficiency; Volunteers

The current study aimed to investigate the molecular mechanisms of metformin and vitamin D3-induced nephroprotection in a metabolic syndrome (MetS) rat model, evaluating the capacity of vitamin D3 to potentiate metformin action. MetS was induced by 10% fructose in drinking water and 3% salt in the diet. After 6 weeks, serum lipid profile and uric acid were measured, an oral glucose tolerance test (OGTT) was performed, and kidney function was investigated. In conjunction with the same concentrations of fructose and salt feeding, MetS rats with significant weight gain, dyslipidemia, hyperuricemia, and dysglycemia were treated orally with metformin (200 mg/kg), vitamin D3 (10 µg/kg), or both daily for 6 weeks. At the end of the study period, anthropometrical parameters were recorded, OGTT was reperformed, urine and blood samples were collected, and tissue samples were harvested at sacrifice. MetS rats showed dramatically declined renal function, enhanced intrarenal oxidative stress and inflammation, and extravagant renal histopathological damage with interstitial fibrosis. Metformin and vitamin D3 significantly reversed all the aforementioned deleterious effects in MetS rats. The study has verified the nephroprotective effects of metformin and vitamin D3 in MetS, accentuating the critical role of AMP-activated protein kinase/sirtuin-1 activation and dipeptidyl peptidase-4 inhibition. Given the synergistic effects of the combination, vitamin D3 is worth being investigated as an additional therapeutic agent for preventing MetS-induced nephropathy.

Topics: AMP-Activated Protein Kinases; Animals; Cholecalciferol; Dipeptidyl-Peptidase IV Inhibitors; Male; Metabolic Syndrome; Metformin; Rats

Cholecalciferol (D3) may improve inflammation, and thus provide protection from cardiometabolic diseases (CMD), although controversy remains. Omega-3 fatty acids (ω-3FA) may also prevent the development of CMD, but the combined effects of ω-3FA and D3 are not fully understood.. We determined the chronic independent and combined effects of D3 and ω-3FA on body weight, glucose homeostasis, and markers of inflammation in obese mice.. We gave 8-week-old male C57BL/6J mice, which had been fed a high-fat, high-sucrose (HF) diet (65.5% kcal fat, 19.8% kcal carbohydrate, and 14% kcal protein) for 12 weeks, either a standard D3 dose (+SD3; 1400 IU D3/kg diet) or a high D3 dose (+HD3; 15,000 IU D3/kg diet). We fed 1 +SD3 group and 1 +HD3 group with 4.36% (w/w) fish oil (+ω-3FA; 44% eicosapentaenoic acid, 25% docosahexaenoic acid), and fed the other 2 groups with corn oil [+omega-6 fatty acids (ω-6FA)]. A fifth group was fed a low-fat (LF; 15.5% kcal) diet. LF and HF+ω-6+SD3 differences were tested by a Student's t-test and HF treatment differences were tested by a 2-way ANOVA.. D3 supplementation in the +HD3 groups did not significantly increase plasma total 25-hydroxyvitamin D and 25-hydroxyvitamin D3 [25(OH)D3] versus the +SD3 groups, but it increased 3-epi-25-hydroxyvitamin D3 levels by 3.4 ng/mL in the HF+ω-6+HD3 group and 4.0 ng/mL in the HF+ω-3+HD3 group, representing 30% and 70%, respectively, of the total 25(OH)D3 increase. Energy expenditure increased in those mice fed diets +ω-3FA, by 3.9% in the HF+ω-3+SD3 group and 7.4% in the HF+ω-3+HD3 group, but it did not translate into lower body weight. The glucose tolerance curves of the HF+ω-3+SD3 and HF+ω-3+HD3 groups were improved by 11% and 17%, respectively, as compared to the respective +ω-6FA groups. D3 supplementation, within the ω-3FA groups, altered the gut microbiota by increasing the abundance of S24-7 and Lachnospiraceae taxa compared to the standard dose, while within the ω-6FA groups, D3 supplementation did not modulate specific taxa.. Overall, D3 supplementation does not prevent CMD or enhance the beneficial effects of ω-3FA in vitamin D-sufficient obese mice.

Topics: Animals; Cholecalciferol; Diet, High-Fat; Dietary Sucrose; Dietary Supplements; Drug Synergism; Fatty Acids, Omega-3; Glucose Intolerance; Humans; Leptin; Liver; Male; Metabolic Syndrome; Mice; Mice, Inbred C57BL; Mice, Obese; Obesity; Random Allocation

The purpose of the study is to increase the effectiveness of treatment of metabolic syndrome (MS) in young patients with vitamin D deficiency.. The study involved 54 patients with MS and vitamin D deficiency (50% of women, 50% of men), aged 2044years. To assess the concentration of melatonin at a young age, a control group of 42 practically healthy volunteers with comparable demographic characteristics with no signs of MS was formed.. In patients with MS and vitamin D deficiency, there was a significant decrease in the average daily level of 6-sulfatoxymelatonin in the urine by 3.7 times, compared with the group of individuals without MS. Patients with MS and vitamin D deficiency (n=54) were randomly assigned to two groups with comparable clinical and demographic characteristics. Patients of the 1st group (n=27) observed dietary recommendations and took the drug Metformin at a dose of 1700 mg/day for 12 months. In the 2nd group (n=27), in addition to the one indicated in the 1st treatment group, correction of vitamin D deficiency was performed (a micelled preparation of cholecalciferol at a dose of 4000 IU/day, for 6 months, then 2000 IU/day for another 6 months) and the level of melatonin (melatonin preparation at a dose of 3 mg/day for 6 months). After treatment in young patients with MS, there was a significant change in the median of the studied parameters in all therapeutic groups, but more pronounced dynamics was observed in group 2 in terms of: WC in women, BMI, insulin resistance index, LDL cholesterol, TG, hs-CRP, hs-TNF-, IL-6, leptin.. To increase the effectiveness of MS treatment in young patients with vitamin D deficiency, it is necessary to determine the level of melatonin (urinary 6-sulfatoxymelatonin) and, if it decreases, carry out correction of melatonin and 25 (OH) vitamin D in addition to the standard therapy of this syndrome.. Цель.Повысить эффективность лечения метаболического синдромом (МС) у молодых пациентов с дефицитом витамина D. Материалы и методы.В исследовании участвовали 54 пациента с МС и дефицитом витамина D (50% женщин, 50% мужчин), в возрасте 2044 лет. Для оценки концентрации мелатонина в молодом возрасте сформирована контрольная группа из 42 практически здоровых добровольцев с сопоставимыми демографическими характеристиками без признаков МС. Результаты.У пациентов с МС и дефицитом витамина D наблюдали достоверное снижение среднесуточного уровня 6-сульфатоксимелатонина в моче в 3,7 раза по сравнению с группой лиц без МС. Пациенты с МС и дефицитом витамина D (n=54) рандомизированы на две сопоставимые по клинико-демографическим характеристикам группы. Пациенты 1-й группы (n=27) соблюдали диетические рекомендации и принимали препарат метформин в дозе 1700 мг/сут в течение 12 мес. Во 2-й группе (n=27) дополнительно к указанному в 1-й группе лечения проводили коррекцию дефицита витамина D (мицеллированным препаратом колекальциферола в дозировке 4000 МЕ/сут в течение 6 мес, затем 2000 МЕ/сут еще в течение 6 мес) и уровня мелатонина (препаратом мелатонина в дозе 3 мг/сут в течение 6 мес). После проведенной терапии у молодых пациентов с МС отметили значимое изменение медианы изучаемых показателей во всех терапевтических группах, но более выраженную динамику наблюдали во 2-й группе по показателям: окружность талии у женщин, индекс массы тела, индекс инсулинорезистентности, холестерин липопротеидов низкой плотности, триглицериды, высокочувствительный С-реактивный белок, высокочувствительный фактор некроза опухоли, интерлейкин-6, лептин. Заключение.Для повышения эффективности лечения МС у молодых пациентов с дефицитом витамина D необходимо определять уровень мелатонина (6-сульфатоксимелатонина мочи) и при его снижении проводить коррекцию мелатонина и 25 (ОН) витамина D дополнительно к стандартной терапии данного синдрома.

Topics: Cholecalciferol; Dietary Supplements; Female; Humans; Male; Metabolic Syndrome; Vitamin D Deficiency; Vitamins

The growing number of overweight and obese individuals is an alarming global problem; these conditions are risk factors for the development of health problems such as metabolic syndrome (MetS), type-2 diabetes, atherosclerosis, and cardiovascular disease. Numerous studies have suggested that vitamin D₃ deficiency plays a role in the pathogenesis of MetS. The aim of this study was to analyze the relationship between MetS and vitamin D₃ levels in women. Laboratory analysis demonstrated that only 26.89% of the participants had vitamin D₃ levels close to normal, and waist-to-hip ratio (WHR) measurements revealed android obesity in 75.63% of the women. The menstruating women more often suffered from vitamin D₃ deficiency, and less often had elevated vitamin D₃ levels. The conclusions are as follows: (1) There were no statistically significant relationships between vitamin D₃ levels and MetS parameters, namely the level of triglycerides, the levels of low- and high-density lipoproteins (LDL and HDL), the level of total cholesterol, and systolic and diastolic blood pressure (SBP and DBP). Vitamin D deficiency was only observed in the women with abdominal obesity. (2) Low vitamin D₃ levels were typical of perimenopausal women. Age was a variable correlating with vitamin D. (3) The presence of menstrual cycles was an important contributor to vitamin D levels. Vitamin D deficiency was significantly more common in the menstruating women.

Topics: Adult; Cholecalciferol; Female; Humans; Menstrual Cycle; Metabolic Syndrome; Middle Aged; Obesity; Poland; Risk Factors; Vitamin D Deficiency; Waist-Hip Ratio

The aim of this study was to examine the effects of cholecalciferol on systemic inflammation and memory in the setting of fatty liver disease in rats.. To induce the development of fatty liver disease, the rats were fed a 35% fructose solution over 8 weeks. Group I (n=6) was designated as the control group and fed with standard rat chow. Group II (n=6) was provided with, standard rat chow, and 0.3 μg/kg/day of oral cholecalciferol over a duration of 2 weeks. In addition to standard rat chow, group III (n=6) and group IV (n=6) were given 4 mL of the 35% fructose solution per day via oral gavage for 8 weeks. However, group IV was also given 0.3 μg/kg/day of oral cholecalciferol over 2 weeks. After the treatment period, passive avoidance tasks were performed by all groups. The liver and brain were harvested for subsequent biochemical and histopathologic analyses.. The development of fatty liver extends the memory latency period of passively avoiding tasks after 1 trial. Moreover, there were increases in brain TNF-α and plasma MDA levels according to two-way analysis of variance. Cholecalciferol supplementation decreased the latency period of passively avoiding tasks in rats with hepatosteatosis, and also significantly reduced brain TNF-α and plasma MDA levels.. Fatty liver may contribute to the development of systemic inflammation, which affects cognition and causes deficits in memory; however, the anti-inflammatory and antioxidant properties of vitamin D may improve the cognitive function of rats with hepatosteatosis.

Topics: Administration, Oral; Animals; Avoidance Learning; Cholecalciferol; Cognition Disorders; Disease Models, Animal; Fatty Liver; Inflammation; Inflammation Mediators; Male; Metabolic Syndrome; Rats; Rats, Sprague-Dawley

Previous studies have linked vitamin D deficiency to hypertension, dyslipidemia, diabetes mellitus, and cardiovascular disease. The aim of this study was to investigate the short-term effects of vitamin D₃ supplementation on weight and glucose and lipid metabolism in antipsychotic-treated patients. A total of 19 schizophrenic or schizoaffective patients (BMI>27 kg/m²) taking atypical antipsychotics were recruited and dispensed a 2000 IU daily dose of vitamin D₃. On comparing baseline with week 8 (study end) results, we found a statistically significant increase in vitamin D₃ and total vitamin D levels but no statistically significant changes in weight, glucose, or lipids measurements. Patients whose vitamin D₃ level at week 8 was 30 ng/ml or more achieved a significantly greater decrease in total cholesterol levels compared with those whose week 8 vitamin D₃ measurement was less than 30 ng/ml. These results suggest that a randomized trial with a longer follow-up period would be helpful in further evaluating the effects of vitamin D₃ on weight, lipid metabolism, and on components of metabolic syndrome in antipsychotic-treated patients.

Topics: Adult; Aged; Antipsychotic Agents; Body Mass Index; Cholecalciferol; Dietary Supplements; Female; Humans; Hypercholesterolemia; Male; Massachusetts; Metabolic Syndrome; Middle Aged; Overweight; Pilot Projects; Psychiatric Status Rating Scales; Psychotic Disorders; Risk Factors; Schizophrenia; Vitamin D Deficiency

Topics: Adolescent; Adult; Case-Control Studies; Cholecalciferol; Cross-Sectional Studies; Female; Humans; India; Metabolic Syndrome; Polycystic Ovary Syndrome; Vitamin D Deficiency; Young Adult

Low vitamin D (25 OH vitamin D) is implicated in the development of diabetes and the metabolic syndrome. We examined whether hypovitaminosis D has a clinically significant impact on glycaemia, metabolic status and inflammatory markers in Chinese patients with established type 2 diabetes.. Characteristics of 109 patients aged over 50 years were stratified by 25 OH vitamin D status. Patients identified as 25 OH vitamin D deficient (or= 0.4 for all) and no association between 25OHVitD and ferritin or hsCRP (p >or= 0.3 for all). Neither BMI nor the metabolic syndrome affected the incremental rise in 25OHVitD levels during supplementation.. There is no relationship between hypovitaminosis D and metabolic control or inflammatory markers in established type 2 diabetes.This suggests that at least in Chinese populations, the effect of low vitamin D is not clinically significant once diabetes is established. Future 25OHVitD intervention trials should therefore focus on prevention in pre-diabetes.

Topics: Adiposity; Aged; Asian People; Australia; Biomarkers; Body Mass Index; C-Reactive Protein; Calcium; China; Cholecalciferol; Diabetes Mellitus, Type 2; Female; Ferritins; Glycated Hemoglobin; Humans; Inflammation Mediators; Male; Metabolic Syndrome; Middle Aged; Parathyroid Hormone; Phosphates; Time Factors; Treatment Outcome; Vitamin D; Vitamin D Deficiency; Vitamins

Vitamin D insufficiency is widespread, regardless of geographical location. It is particularly prevalent in the elderly and has far-ranging health consequences including: osteoporosis, falls, increased risk of cancer, and altered glucose and lipid metabolism. Increasing evidence strongly supports the benefits of vitamin D supplementation and also reveals that present recommendations are inadequate, especially for older individuals. Although additional studies are still needed to further optimize diagnostic and therapeutic approaches, physicians should consider prescribing cholecalciferol--at least 2000 international units (IU) per day--to all elderly patients. Oral cholecalciferol supplementation at that level is inexpensive, safe, and effective, and has great potential to improve the quality of life of the elderly.

Topics: Accidental Falls; Aged; Cholecalciferol; Fractures, Bone; Humans; Inflammation; Metabolic Syndrome; Neoplasms; Osteoporosis; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency; Vitamins