The Effect of Vitamin D Supplementation on Adiposity, Blood Glycated Hemoglobin, Serum Leptin and Tumor Necrosis Factor-α in Type 2 Diabetic Patients Vitamin D deficiency, serum leptin and osteoprotegerin levels in older diabetic patients: an input to new research avenues Not a simple fat-soluble vitamin: Changes in serum 25-(OH)D levels are predicted by adiposity and adipocytokines in older adults. Investigating the causal effect of vitamin D on serum adiponectin using a mendelian randomization approach Effect of high doses of vitamin D on arterial properties, adiponectin, leptin and glucose homeostasis in type 2 diabetic patients. Effect of vitamin D supplementation on selected inflammatory biomarkers in older adults: a secondary analysis of data from a randomised, placebo-controlled trial. Effect of vitamin D deficiency and replacement on endothelial function in asymptomatic subjects. Multivariate Path Analysis of Serum 25-Hydroxyvitamin D Concentration, Inflammation, and Risk of Type 2 Diabetes Mellitus Effect of a single, oral, high-dose vitamin D supplementation on endothelial function in patients with peripheral arterial disease: a randomised controlled pilot study. Large Doses of Vitamin D Fail to Increase 25-Hydroxyvitamin D Levels or to Alter Cardiovascular Risk Factors in Obese Adolescents: A Pilot Study. Overview of the Cohort Consortium Vitamin D Pooling Project of Rarer Cancers Serum 25-Hydroxyvitamin D Concentrations and Depressive Symptoms among Young Adult Men and Women Association of low serum 25-hydroxyvitamin D levels and high arterial blood pressure in the elderly. Consumption of vitamin D-fortified yogurt drink increased leptin and ghrelin levels but reduced leptin to ghrelin ratio in type 2 diabetes patients: a single blind randomized controlled trial Effect of Therapeutic Dose of Vitamin D on Serum Adiponectin and Glycemia in Vitamin D-Insufficient or Deficient Type 2 Diabetic Patients Is serum vitamin D levels associated with disability in patients with newly diagnosed multiple sclerosis? Effect of acute and chronic vitamin D administration on systemic renin angiotensin system in essential hypertensives and controls
Background : Since tumor necrosis factor-α ( TNF-α ) could be one of the risk factors at the development of diabetes complications ; as well as serum leptin deficiency is related to increased susceptibility to infections in diabetic patients , they are potential indices from the preventive medicine viewpoint . This study was conducted to represent the effect of supplemental vitamin D3 on serum leptin , TNF-α and adiposity in type 2 diabetic patients . Methods : In this r and omized double-blind placebo-controlled trial , study sample was selected through type 2 diabetic patients ( n = 51 ) . A total of 26 patients were orally supplemented by vitamin D3 ( 400 IU/d ) ( vitamin D group ) and 25 patients by placebo ( placebo group ) for 14 weeks . The blood glycated hemoglobin ( HbA1c ) and the serum ionized Ca , leptin , TNF-α , and serum 25-hydroxyvitamin D ( 25[OH ] D ) were measured at the two groups in the baseline and postintervention stages . Results : It was shown that despite of theplacebo group , serum 25(OH ) D and serum leptin was significantly increased ( P = 0.001 and P = 0.002 , respectively ) , while serum TNF-α was decreased significantly ( P = 0.001 ) in vitamin D group . The remaining parameters , including body fat mass and HbA1c had no alterations between baseline and postintervention stages in vitamin D group . Conclusions : This study may advocate vitamin D supplementation among type 2 diabetic patients due to its beneficial effects on prevention of diabetes complications The aim of this study was to assess the effects of single oral bolus of 300,000 IU Vitamin D3 on serum levels and on bone and metabolic parameters in diabetic patients . This study is a Phase IV , r and omized , double-blind , placebo-controlled , monocenter clinical trial . Thirty patients , 60 years or older , with type 2 diabetes mellitus , and diabetic foot complications , were enrolled and monitored for 24 weeks : 14 were treated with Vitamin D3 and 16 with placebo . Parameters including glucose , adiponectin , leptin , osteoprotegerin ( OPG ) , 25-hydroxyvitamin D [ 25(OH)D ] , beta-CrossLaps , osteocalcin , bone-specific isoenzyme of alkaline phosphatase , tumor necrosis factor-α and parathyroid hormone were measured at screening and baseline and 12 and 24 weeks after treatment . Analysis of covariance was used to compare treatment groups . Analysis of the data detected a significant increase in 25(OH)D serum levels both at 12 and 24 weeks with respect to baseline values only in the treated patients . Significant variations with respect to baseline values were noted in OPG ( P = 0.0085 ) and in leptin ( P = 0.0442 ) levels : these were lower in the placebo group at week 24 but higher in the treated group . Vitamin D3 supplementation significantly increased serum leptin and OPG levels . Further , large-scale clinical trials are warranted to confirm these results OBJECTIVE To determine the associations between body adiposity and change in serum 25-(OH)D levels over 2.6 years , and if these associations are mediated by metabolic and inflammatory factors in older adults . METHODS This is a longitudinal study of 859 r and omly selected subjects ( mean 62 years , range 51 - 80 , 49 % women ) . Serum 25-hydroxyvitamin D [ 25-(OH)D ] was assessed by radioimmunoassay at baseline and 2.6 years later . Baseline serum level of leptin  was assessed by radioimmunoassay and interleukin (IL)-6 by a chemiluminescent immunoassay in the first 183 subjects . RESULTS In multivariable analyses , body mass index , trunk fat percentage and waist-to-hip ratio were significant predictors of increased incident vitamin D deficiency [ a 25-(OH)D < 50 nmol L⁻¹ at follow-up when ≥50 nmol L⁻¹ at baseline ] and decreased recovery of vitamin D deficiency [ a 25-(OH)D ≥ 50 nmol L⁻¹ at follow-up when < 50 nmol L⁻¹ at baseline ] . Change in 25-(OH)D levels per annum was also independently predicted by baseline leptin ( β : -0.09/unit , 95 % CI : -0.17 , -0.03 ) , IL-6 ( β : -0.68/quartile , 95 % CI : -1.35 , -0.02 ) and total cholesterol/high-density lipoprotein ( HDL ) ratio ( β : -0.51 , 95 % CI : -0.88 , -0.14 ) . The associations between body adiposity measures and change in 25-(OH)D completely disappeared after adjustment for leptin , diminished after adjustment for IL-6 , but remained unchanged after adjustment for total cholesterol/HDL ratio . All associations were independent of season and sun exposure . CONCLUSIONS Body fat is not simply a passive reservoir for 25-(OH)D. In addition to season and sun exposure , 25-(OH)D levels appear to be determined by metabolic and , to a lesser extent , inflammatory factors , and these appear to mediate the effects of adiposity on change in Background / Objectives : The aim was to examine the causal effect of vitamin D on serum adiponectin using a multiple instrument Mendelian r and omization approach . Subjects/ Methods :  Serum 25-hydroxy vitamin D ( 25(OH)D ) and serum total or high molecular weight ( HMW ) adiponectin  were measured in two Danish population -based studies : the Inter99 study ( 6405 adults , 30–60 years ) conducted in 1999–2001 , and the MONICA10 study ( 2656 adults , 41–71 years ) conducted in 1993–1994 . Results : In the Inter99 study , serum 25(OH)D was positively associated with total adiponectin ( the effect estimate in % per doubling of 25(OH)D was 4.78 , 95 % CI : 1.96 , 7.68 , P<0.001 ) . Using variations in the vitamin D-binding protein gene and the filaggrin gene as instrumental variables , the causal effect in % was estimated to 61.46 , 95 % CI : 17.51 , 120.28 , P=0.003 higher adiponectin per doubling of 25(OH)D. In the MONICA10 cohort , no significant association was observed between the serum concentrations of 25(OH)D and HMW adiponectin ( the effect estimate in % per doubling of 25(OH)D was −1.51 , 95 % CI : −5.80 , 2.98 , P=0.50 ) , although the instrumental variables analysis to some extent supported a positive causal association ( the effect estimate in % per doubling of 25(OH)D was 37.13 , 95 % CI : −3.67 , 95.20 , P=0.080 ) . Conclusions : The results indicate a possible causal association between serum 25(OH)D and total adiponectin . However , the association was not replicated for HMW adiponectin . Thus , further studies are needed to confirm a causal relationship BACKGROUND & AIMS Vitamin D supplementation has the potential to alleviate the cardiovascular damage in diabetic patients . The present study was design ed to evaluate long term impact of high doses of vitamin D on arterial properties , glucose homeostasis , adiponectin and leptin in patients with type 2 diabetes mellitus . METHODS AND RESULTS In r and omized , placebo-controlled study 47 diabetic patients were assigned into two groups : Group 1 received oral daily supplementation with vitamin D at a dose of 1000 U/day for 12 months . Group 2 received matching placebo capsules . Blood sampling for metabolic parameters , including fasting glucose , lipid profile , HbA1C , insulin , hs-CRP , 25 OH Vit D , adiponectin and leptin was performed at baseline and at the end of the study . Insulin resistance was assessed by homeostasis model assessment ( HOMA-IR ) . Central aortic augmentation index ( AI ) was evaluated using SphygmoCor . RESULTS The two groups were similar at baseline in terms of hemodynamic parameters . After 12 months , AI decreased significantly during the treatment period in patients received vitamin D ( p < 0.0001 ) and did not change in placebo group . Glucose homeostasis parameters , leptin as well as leptin adiponectin ratio did not change in both groups . 25 OH Vit D level significantly increased ( p = 0.022 ) and circulating adiponectin marginally increased ( p = 0.065 ) during 12 month treatment period in active treatment and did not change in placebo group . CONCLUSIONS High doses of  vitamin D supplementation in diabetic patients was associated with significant decrease in AI during one year treatment . This beneficial vascular effect was not associated with improvement in glucose homeostasis parameters 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 aim ed to determine the effect of supplementary vitamin D using secondary data from a population -based , r and omised , 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 r and omly selected from the electoral roll and were r and omised 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 sample s 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 CONTEXT Vitamin D receptors are present in many tissues . Hypovitaminosis D is considered to be a risk factor for atherosclerosis . OBJECTIVE This study explores the effects of vitamin D replacement on insulin sensitivity , endothelial function , inflammation , oxidative stress , and leptin in vitamin D-deficient subjects . DESIGN , SETTING , AND PATIENTS 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 i m 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 ) . RESULTS 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 ) . CONCLUSIONS 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 Background and Aims . Despite growing interest in the protective role that vitamin D may have in health outcomes , little research has examined the mechanisms underlying this role . This study aim ed to test two hypotheses : ( 1 ) serum 25-hydroxyvitamin D [ 25(OH)D ] is inversely associated with type 2 diabetes mellitus ( T2DM ) and elevated hemoglobin A1c ; ( 2 ) these associations are mediated by serum C-reactive protein ( CRP ) . Methods . Participants aged 20 and older in 2001–2006 National Health and Nutrition Examination Surveys ( n = 8,655 ) with measures of serum 25(OH)D , CRP , hemoglobin A1c , and other important covariates were included in the present study . Logistic regression and path analysis methods were applied to test the study hypotheses . Results . Decreased serum 25(OH)D concentration was significantly associated with increased odds of T2DM .  In males , an estimated 14.9 % of the association between 25(OH)D and hemoglobin A1c was mediated by serum CRP . However , this mediation effect was not observed in females . Conclusion . Using a nationally representative sample , the present study extends previous research and provides new evidence that the effect of  decreased serum vitamin D concentration on T2DM may proceed through increased systemic inflammation in males . Longitudinal studies and r and omized control trials are needed to confirm the present findings OBJECTIVE Apart from its role in bone metabolism , vitamin D may also influence cardiovascular disease . The objective of this study was : ( 1 ) to determine the effect of a single , oral , high-dose vitamin D supplementation on endothelial function and arterial stiffness in patients with peripheral arterial disease ( PAD ) and ( 2 ) to investigate the impact of this supplementation on coagulation and inflammation parameters . METHODS In this double-blind , placebo-controlled , interventional pilot study , we screened 76 Caucasian patients with PAD for vitamin D deficiency . Sixty-two were r and omised to receive a single , oral supplementation of 100,000 IU vitamin D3 or placebo . At baseline and after 1 month , we measured serum vitamin D and parathormone levels , and surrogate parameters for cardiovascular disease . RESULTS Sixty-five of 76 patients ( 86 % ) had low 25-hydroxyvitamin D levels ( < 30 ng ml(-1 ) ) ; of those , 62 agreed to participate in the study . At baseline , only parathormone was related to vitamin D. In supplemented patients , vitamin D levels increased from 16.3 ± 6.7 to 24.3 ± 6.2 ng ml(-1 ) ( P < 0.001 ) , with wide variations between single patients ; in the placebo group vitamin levels did not change . Seasonal factors accounted for a decrease of vitamin D levels by 8 ng ml(-1 ) between summer and winter . After 1 month , none of the measured parameters was influenced by vitamin substitution . CONCLUSION In this pilot study , most patients with PAD were vitamin D deficient . Vitamin D supplementation  increased serum 25-hydroxyvitamin D without influencing endothelial function , arterial stiffness , coagulation and inflammation parameters , although the study was underpowered for definite conclusions PURPOSE Vitamin D deficiency and cardiometabolic risk factors are common in obese adolescents . Observational studies demonstrate an inverse relationship among serum 25-hydroxyvitamin D ( 25OHD ) and obesity , insulin resistance , and inflammatory cytokines . This pilot study explores if vitamin D supplementation could reduce serum concentrations of inflammatory cytokines ( interleukin [ IL ] 6 , IL-10 , tumor necrosis factor α ) , adiponectin , lipids , hemoglobin A1C , and high-sensitivity C-reactive protein ( hs-CRP ) . A secondary aim was to determine the associations between baseline serum 25OHD concentrations and body mass index ( BMI ) , hs-CRP , inflammatory cytokines , and lipids . METHODS Overweight and obese adolescents enrolled in this 24-week , r and omized , double-blind study were given 150,000 IU ergocalciferol or placebo at baseline and 12 weeks . Outcome measurements included serum 25OHD , inflammatory cytokines , adiponectin , hs-CRP , lipids , hemoglobin A1C , and BMI at baseline , 12 , and 24 weeks . RESULTS Of 40 participants , 31 ( 78 % ) completed the study . Mean ± st and ard error 25OHD levels were similar in vitamin D and placebo groups at baseline ( 19.6 ± 5.3 vs. 25.8 ± 10.8 ng/mL ) and 24 weeks ( 20.1 ± 3.4 vs. 24.6 ± 8.4 ng/mL ) . Inflammatory and cardiovascular markers were not significantly different between groups at 24 weeks . Serum 25OHD at baseline was associated with BMI ( r = -.44 [ 95 % confidence interval , -.66 to -.15 ] ) but not with other outcome measures . CONCLUSIONS Supplementation with vitamin D at 150,000 IU every 3 months failed to increase serum 25OHD or alter inflammatory markers and lipids in overweight and obese youth . Further studies are needed to establish the dose of vitamin D required to increase 25OHD and determine potential effects on metabolic risk factors in obese teens The Cohort Consortium Vitamin D Pooling Project of Rarer Cancers ( VDPP ) brought together 10 cohorts to conduct a prospect i ve study of the association between vitamin D status , measured as serum concentrations of 25-hydroxyvitamin D ( 25(OH)D ) , and the development of 7 rarer cancer sites : endometrial , esophageal , gastric , kidney , non-Hodgkin lymphoma , ovarian , and pancreatic cancers . The cohorts come from 3 continents , with participants from a wide range of latitude who are racially diverse . Across each cancer site , there was no evidence of a protective association between higher concentrations of 25-hydroxyvitamin D ( > 75 nmol/L ) and cancer outcome . An increased risk at very high levels ( ≥100 nmol/L ) was noted for pancreatic cancer , confirming previous reports . The articles included in this issue detail the overall design and governance of the project , correlates of vitamin D status , and results from the cancer site-specific investigations . The Vitamin D Pooling Project realizes a major goal of consortium efforts , namely , to rigorously test hypotheses for rarer cancer outcomes that may not be adequately addressed in any one prospect i ve cohort study . The results of this study have application for the planning and conduct of intervention trials , especially in determining potential risks There has been an increased interest in the role of vitamin D in depression ; however , there have been few studies conducted in younger population groups . Our aim was to investigate the association between vitamin D status and depressive symptoms in a non- clinical young adult sample living in Dunedin , New Zeal and . A cross-sectional sample of 615 young adults completed a question naire including demographics and the  Centre  for Epidemiological Studies Depression Scale ( CES-D ) . Height , weight and a blood sample for 25-hydroxyvitamin D [ 25(OH)D ] was obtained . Serum 25(OH)D was used to predict depression scores , adjusting for potential confounders including time spent outdoors for 13 consecutive days , BMI , age , sex and ethnicity . Prevalence of low vitamin D was high even in this age group , and serum 25(OH)D was negatively associated with depression symptoms before and after adjustment . When investigating the relationship between the presence versus absence of depressive symptoms and quartiles of 25(OH)D , participants in the lowest quartile were more likely to report depressive symptoms compared with those in the highest quartile . Although our findings suggest that vitamin D is a predictor of depression symptomatology , even when controlling for time spent outdoors , a r and omised controlled trial in this young adult target group is needed to confirm the association BACKGROUND Vitamin D and calcium metabolism are involved in vascular smooth muscle cell proliferation , endothelial function and blood pressure ( BP ) regulation . Their physiopathology has been a matter of intensive clinical investigation with variable and sometimes contradictory results . Vitamin D insufficiency is highly prevalent in the general population , particularly among the elderly . We evaluated the association between serum 25(OH)-D levels and arterial BP in this population . METHODS An epidemiological cross-sectional study was design ed to analyse the prevalence of hypovitaminosis D ( ' D'AVIS ' study ) in our reference area . The study was performed on a representative r and om sample of the population over 64 years of age obtained from five primary health care areas . A medical record , arterial BP and biological analysis : serum 25(OH)-D , iPTH , creatinine , urea , calcium , albumin were obtained . RESULTS A total of 237 subjects ( 53 % women ) , aged between 64 and 93 ( mean 71.7 + /- 5.3 ) , were evaluated . The mean serum 25(OH)-D levels were 17.21 + /- 7.57 ng/ml ( interval 5 - 54 ; 86 % had < 25 ng/ml ) . The mean BP was 138.8 + /- 14/80 + /- 7.4 mmHg , and 46 % were on antihypertensive treatment . A significant negative association was observed between serum 25(OH)-D levels and systolic ( r = -0.153 , P = 0.018 ) and diastolic BP ( r = -0.152 , P = 0.019 ) . This association persisted after controlling for possible confounders in the multivariate analyses . CONCLUSIONS Low serum 25(OH)-D levels were inversely and independently associated with BP . Supplemental measures to prevent hypovitaminosis D in this population would be important , not only to protect the skeletal system but also for the possible beneficial effects on the cardiovascular system and the BP regulation Purpose This study aim ed to evaluate the effect of daily consumption of vitamin D-fortified yogurt drink ( doogh ) in comparison with plain doogh on appetite-regulating hormones including leptin and ghrelin in type 2 diabetes ( T2D ) patients . Methods In a single blind r and omized clinical trial , subjects with T2D were r and omly allocated to one of the two groups and received either vitamin D3-fortified doogh ( FD ; containing 170 mg calcium and 500 IU/250 mL , n2 = 50 ) or plain doogh ( PD ; containing 170 mg calcium and no vitamin D/250 mL , n1 = 50 ) twice a day for 12 weeks . Leptin and ghrelin were evaluated at the beginning and after 12 weeks of intervention . Results The intervention result ed in a significant improvement of circulating 25(OH)D , fasting glucose , Quantitative Insulin Check Index ( QUICKI ) , hs-CRP , in FD compared with PD group . A significant rise in both serum leptin ( + 1.3 ± 7.2 mg/L ; p = 0.013 ) and ghrelin ( 10.1 ± 26.1 ng/L ; p = 0.012 ) was observed in FD group . A between-group difference for ghrelin changes ( p = 0.029 ) remained significant after adjusting for changes QUICKI ( p = 0.039 ) , body mass index ( p = 0.034 ) and hs-CRP ( p = 0.022 ) . Despite an increase in both leptin and ghrelin , leptin to ghrelin ( L/G ) ratio actually decreased in FD . Changes of L/G ratio showed a significant between-group difference ( p = 0.036 ) , which remained significant even after adjusting for changes of hs-CRP ( p = 0.028 ) and fat mass ( p = 0.047 ) but disappeared after adjusting for changes of QUICKI ( p = 0.42 ) . Conclusions Daily intake of vitamin D-fortified doogh may increase circulating leptin and ghrelin but L/G ratio may actually decrease . Our results suggest that improving vitamin D may result in an improvement in insulin sensitivity which may finally regulate beneficially appetite hormones . Further studies with adequate power are needed to confirm the results Background : Lower vitamin D status has been reported in diabetic patients . Serum 25-hydroxyvitamin D and adiponectin were inversely associated with type 2 diabetes and insulin resistance . Vitamin D may involve in regulation of the adiponectin levels , which is directly related to insulin sensitivity . Objectives : The aim of this study was to investigate the effect of therapeutic dose of vitamin D on serum adiponectin and insulin resistance in vitamin D-insufficient or deficient type 2 diabetic patients . Material s and Methods : This double-blind , r and omized , clinical trial was conducted on 81 type 2 diabetic patients with vitamin D level of 10 - 30 ng/mL. Intervention was 50000 IU vitamin D or placebo once a week for 8 weeks . At the beginning and end of the study , blood sample s were collected after 12 hours of fasting and serum glucose , insulin , 25-hydroxyvitamin D , and adiponectin were measured . Insulin resistance was calculated by homeostasis model assessment ( HOMA-IR ) . Results : After 8-week intervention , serum 25-hydroxyvitamin D significantly increased and reached the normal levels in patients receiving vitamin D ( P < 0.001 ) and the levels of fasting serum glucose , insulin , and HOMA-IR were significantly decreased ( P = 0.04 , 0.02 and 0.007 , respectively ) . No significant changes were observed in these levels in the placebo group . Significant differences were observed in mean changes in the above-mentioned variables between the two groups ( P = 0.01 , 0.04 and 0.006 , respectively ) . No significant changes were found in serum adiponectin in the vitamin D and placebo groups ( P = 0.83 ) . Conclusions : Therapeutic dose of vitamin D can improve vitamin D status and glycemic indicators . But it seems that an 8-week intervention period was not sufficient to reveal the possible effects of vitamin D on serum adiponectin levels Background Although the precise etiology of multiple sclerosis ( MS ) is unknown , it seems that both genetic and environmental factors are important . Recent studies suggest that low serum vitamin D levels are important environmental factor in MS . The aim of this study was to compare the serum levels of vitamin D between MS patients and healthy subjects , and to determine its association with disability  in MS patients . Methods In this cross-sectional study , a total of 52 patients with MS were r and omly recruited and matched for age and sex with 52 healthy subjects .  Demographic characteristics and serum vitamin D levels for both groups , as well as duration of disease Exp and ed Disability Status Scale ( EDSS ) for MS patients were evaluated . Statistical analysis was performed by independent sample s t-test and multiple linear regression analysis . Results The mean serum vitamin D levels were 26.5 ± 16.3 ng/ml in MS patients vs. 37.1 ±19.7 in healthy subjects ( P = 0.003 ) . A linear regression analysis showed no significant association between vitamin D levels and EDSS score of patients with MS ( P = 0.345 ) , after adjusting for the covariates . Conclusion Our findings did not suggest a protective association for serum vitamin D levels against disability in MS patients Aim : To investigate the systemic renin-an-giotensin system ( RAS ) in essential hypertensives ( EH ) and controls ( C ) after short- and long-term vitamin D receptor activation . Design : Ten consecutive EH ( under controlled low-salt diet ) and 10 C underwent calcitriol administration ( 0.25 µg bid ) for 1 week ( Group A ) . Eighteen consecutive EH under angiotensin II receptor antagonist therapy  received a single oral dose of 300,000 IU of cholecalciferol and were followed up for 8 weeks ( Group B ) . Methods : In basal conditions and at the end of the study ( 1 week in Group A and 8 weeks in Group B ) , plasma renin activity ( PRA ) , plasma active renin , aldosterone , and angiotensin II were evaluated , as well as blood pressure , plasma 25-hy-droxyvitamin D [ 25(OH)D ] , 1,25-dihydroxyvitamin D [ 1,25(OH)2D ] , and PTH . Results : In Group A , plasma 25(OH)D levels in EH and C were below the normal range , although lower levels were found in the former . No association between basal plasma 25(OH)D or 1,25(OH)2D levels and blood pressure values or RAS components was observed either in the whole group or in the two subgroups . Calcitriol administration did not affect any RAS parameter either in EH or in C. In Group B , cholecalciferol significantly increased 25(OH)D and 1,25(OH)2D levels without interfering with the angiotensin II receptor antagonist-induced increase in RAS components . No correlation was found between plasma 25(OH)D or 1,25(OH)2D levels and blood pressure values or RAS parameters before and after cholecalciferol administration . Conclusions : The present data suggest that , in our experimental conditions , vitamin D receptor activation is unable to influence systemic RAS activity
Current evidence indicates that inverse association between leptin level and 25(OH)D concentration was observed in observational studies , which was not demonstrated in intervention studies with high heterogeneity .
We aim ed to investigate the potential association between vitamin D and serum leptin levels by pooling together the results from observational studies and clinical trials .