Vitamin D supplementation reduces insulin resistance in Japanese adults: a secondary analysis of a double-blind, randomized, placebo-controlled trial. Effect of vitamin D supplementation on glycemic control in patients with type 2 diabetes: a systematic review of interventional studies Supplementation with cholecalciferol does not improve glycaemic control in diabetic subjects with normal serum 25-hydroxyvitamin D levels Vitamin D supplementation reduces insulin resistance in South Asian women living in New Zealand who are insulin resistant and vitamin D deficient - a randomised, placebo-controlled trial. Effect of Vitamin D Supplementation on Obesity‐Induced Insulin Resistance: A Double‐Blind, Randomized, Placebo‐Controlled Trial The effects of oral vitamin D on insulin resistance in pre-diabetic patients A double-blind, randomized, placebo-controlled trial of the short-term effect of vitamin D3 supplementation on insulin sensitivity in apparently healthy, middle-aged, centrally obese men. The Effects of Vitamin D Supplementation on Glucose Control and Insulin Resistance in Patients with Diabetes Type 2: A Randomized Clinical Trial Study Effect of moderate-dose vitamin D supplementation on insulin sensitivity in vitamin D-deficient non-Western immigrants in the Netherlands: a randomized placebo-controlled trial. Vitamin D supplementation has no effect on insulin sensitivity or secretion in vitamin D-deficient, overweight or obese adults: a randomized placebo-controlled trial. Vitamin D supplementation has no effect on insulin resistance assessment in women with polycystic ovary syndrome and vitamin D deficiency. Effects of vitamin D and calcium supplementation on pancreatic β cell function, insulin sensitivity, and glycemia in adults at high risk of diabetes: the Calcium and Vitamin D for Diabetes Mellitus (CaDDM) randomized controlled trial. Serum vitamin-D predicts insulin resistance in individuals with prediabetes Effects of vitamin D on insulin and glucagon secretion in non-insulin-dependent diabetes mellitus. Vitamin D 20,000 IU per Week for Five Years Does Not Prevent Progression From Prediabetes to Diabetes. Effect of vitamin D on insulin resistance and anthropometric parameters in Type 2 diabetes; a randomized double-blind clinical trial A randomized, placebo-controlled trial of vitamin D supplementation to improve glycaemia in overweight and obese African Americans.
Higher circulating 25-hydroxyvitamin D ( 25[OH]D ) concentration has been linked to a lower prevalence of insulin resistance and type 2 diabetes mellitus . However , r and omized controlled trials have not clarified the effect of vitamin D supplementation on insulin resistance in healthy adults . The objective of this study was to assess the effect of vitamin D supplementation for 1 year on insulin resistance ; the study was a secondary analysis of a clinical trial . We hypothesized that increased 25(OH)D concentration after vitamin D supplementation for 1 year would significantly improve insulin resistance .  Ninety-six healthy adults participated in this study , of whom 81 completed the study . The participants r and omly received daily either 420 IU vitamin D3 or placebo in a double-blind manner for 1 year . The levels of fasting insulin , glucose , and other parameters were assessed at baseline and after 1 year of intervention . Homeostasis model assessment of insulin resistance index was calculated from insulin and glucose levels . Visceral fat area and physical activity were also investigated . Serum 25(OH)D and 1,25-dihydroxyvitamin D concentrations were significantly increased by approximately 29.5 nmol/L and 7.0 pg/mL , respectively , after 1-year vitamin D supplementation . After vitamin D supplementation , fasting glucose levels and values of homeostasis model assessment of insulin resistance index significantly decreased from 88.3 to 85.3 mg/dL ( P < .01 ) and 1.17 to 0.84 ( P < .01 ) , respectively , and the results were independent of physical activity and visceral fat accumulation . In conclusion , the present study showed that vitamin D supplementation for 1 year effectively improves fasting glucose level and insulin resistance in healthy Japanese adults Background Diabetes and vitamin D deficiency are global epidemics . Research ers have long been exploring the role of potentially modifiable factors to manage type 2 diabetes . We conducted a systematic review of prospect i ve studies and r and omized controlled trials that involved vitamin D supplementation and specifically intended to study glycemic outcomes related to type 2 diabetes . Methods Two authors independently search ed Medline and PubMed for longitudinal studies that had assessed the effect of vitamin D supplements on glycemic control , insulin resistance and beta-cell dysfunction in patients with diabetes . Results Seventeen r and omized control trials and seven longitudinal studies with a minimum follow-up of one month were included . Results of the various short-term studies ( follow up ≤ 3 months ) suggested that vitamin D supplementation had a positive impact on glycemic control and metabolic parameters such as insulin resistance and beta cell dysfunction . However , the evidence was weak due to the low method ological quality of the studies . There was no significant effect on HbA1c , beta cell function and insulin resistance in the long-term studies ( follow up > 3 months ) . There existed heterogeneity in the methodology of the studies , inclusion criteria , mode of supplementation of vitamin D and the duration of follow up . Conclusions Current evidence based on r and omized controlled trials and longitudinal studies do not support the notion that vitamin D supplementation can improve hyperglycemia , beta cell secretion or insulin sensitivity in patients with type 2 diabetes . Large-scale trials with proper study design , optimal vitamin D supplementation and longer follow up need to be conducted Background Studies have suggested that vitamin D may be important for both insulin sensitivity and insulin secretion , and that supplementation with vitamin D may subsequently prevent development of type 2 diabetes . Aim of the study The objective of the current study was to test the hypothesis that supplementation with vitamin D would improve glycaemic control in subjects with type 2 diabetes . Methods Thirty-six subjects with type 2 diabetes , treated with metformin and bed-time insulin  , were r and omised to supplementation with cholecalciferol ( 40,000 IU per week ) versus placebo for 6 months . Thirty-two subjects participated throughout the entirety of the study . Fasting blood sample s were drawn before and at the end of the 6 month study without the previous bed-time insulin injection . The insulin and metformin doses were not changed throughout the study . Results After 6 months , the fasting glucose , insulin , C-peptide , fructosamine , and HbA1c levels were not significantly different from baseline values . In addition , changes in these parameters ( values at 6 months minus values at baseline ) did not differ between the vitamin D and the placebo group . Conclusions We were not able to demonstrate that vitamin D supplementation had a significant effect on glucose metabolism in subjects with type 2 diabetes but without vitamin D deficiency . Further studies are needed in larger groups of subjects with type 2 diabetes or impaired glucose tolerance , who also exhibit low serum 25-hydroxyvitamin D levels Low serum 25-hydroxyvitamin D ( 25(OH)D ) has been shown to correlate with increased risk of type 2 diabetes . Small , observational studies suggest an action for vitamin D in improving insulin sensitivity and /or insulin secretion . The objective of the present study was to investigate the effect of improved vitamin D status on insulin resistance ( IR ) , utilising r and omised , controlled , double-blind intervention administering 100 microg ( 4000 IU ) vitamin D(3 ) ( n 42 ) or placebo ( n 39 ) daily for 6 months to South Asian women , aged 23 - 68 years , living in Auckl and , New Zeal and . Subjects were insulin resistant - homeostasis model assessment 1 (HOMA1)>1.93 and had serum 25(OH)D concentration < 50 nmol/l . Exclusion criteria included diabetes medication and vitamin D supplementation > 25 microg ( 1000 IU)/d . The HOMA2 computer model was used to calculate outcomes . Median ( 25th , 75th percentiles ) serum 25(OH)D(3 ) increased significantly from 21 ( 11 , 40 ) to 75 ( 55 , 84 ) nmol/l with supplementation . Significant improvements were seen in insulin sensitivity and IR ( P = 0.003 and 0.02 , respectively ) , and fasting insulin decreased ( P = 0.02 ) with supplementation compared with placebo . There was no change in C-peptide with supplementation . IR was most improved when endpoint serum 25(OH)D reached > or = 80 nmol/l . Secondary outcome variables ( lipid profile and high sensitivity C-reactive protein ) were not affected by supplementation . In conclusion , improving vitamin D status in insulin resistant women result ed in improved IR and sensitivity , but no change in insulin secretion . Optimal vitamin D concentrations for reducing IR were shown to be 80 - 119 nmol/l , providing further evidence for an increase in the recommended adequate levels . Registered Trial No. ACTRN12607000642482 Objective The aim was to investigate whether vitamin D supplementation , combined with a hypocaloric diet , could have an independent effect on insulin sensitivity in subjects with both overweight and hypovitaminosis D. Changes from baseline in anthropometric parameters , body composition , glucose tolerance , and insulin secretion were considered as secondary outcomes . Methods Eighteen volunteers who were nondiabetic and vitamin D deficient and had BMI > 25 kg/m2 were r and omized ( 1:1 ) in a double‐blind manner to a hypocaloric diet + either oral cholecalciferol at 25,000 IU/wk or placebo for 3 months . Hyperinsulinemic‐euglycemic clamp to measure insulin sensitivity  was performed at baseline and after intervention . Results Body weight in both groups decreased significantly ( −7.5 % in the vitamin D group and −10 % in the placebo group ; P < 0.05 for both ) , with no between‐group differences . Serum 25‐hydroxyvitamin D levels in the vitamin D group increased considerably ( from 36.7 ± 13.2 nmol/L to 74.8 ± 18.7 nmol/L ; P < 0.001 ) . Insulin sensitivity in the vitamin D group improved ( from 4.6 ± 2.0 to 6.9 ± 3.3 mg·kg−1·min−1 ; P < 0.001 ) , whereas no changes were observed in the placebo group ( from 4.9 ± 1.1 to 5.1 ± 0.3 mg·kg−1·min−1 ; P = 0.84 ) . Conclusions Cholecalciferol supplementation , combined with a weight loss program , significantly improves insulin sensitivity in healthy subjects with obesity and might represent a personalized approach for insulin‐resistant subjects with obesity Background : Some epidemiological and interventional studies have shown the role of vitamin D on insulin secretion and resistance . A previous study in our center showed that intramuscular vitamin D decreases insulin sensitivity in pre-diabetic patients . We investigated the role of oral vitamin D on the insulin sensitivity index and insulin resistance in pre-diabetic patients . Material s and Methods : In a r and omized clinical trial , we divided 45 people with pre-diabetes aged 47.4 ± 6.6 ( range 33 - 61 ) years into three groups : group A subjects treated with 50,000 IU oral vitamin D and 500 mg calcium carbonate ( n = 21 ) , group B subjects treated with a single 300,000 IU intramuscular vitamin D and 500 mg calcium carbonate ( n = 9 ) , and group C subjects treated with 500 mg calcium carbonate alone ( n = 15 ) . Serum 25-hydroxyvitamin D [ 25(OH ) D ] was measured at baseline . If it was less than 75 nmol/l , 50,000 IU vitamin D was given weekly , and if serum 25(OH ) D was more than that , vitamin D was administered every 2 weeks . Before and after 12 weeks of treatment , a 75-g glucose tolerance test was performed . We used paired t-test and analysis of variance ( ANOVA ) to analyze the data . P values less than 0.05 were considered significant . Results : Mean ( SD ) of serum vitamin D increased from 77.5 ± 39.2 to 118.8 ± 56.3 nmol/l ( P = 0.009 ) in group A and from 80 ± 36 to 102.8 ± 43.3 nmol/l ( P = 0.053 ) in group B , and decreased from 44.8 ± 18.3 to 34.6 ± 13.9 nmol/l ( P = 0.06 ) in group C. Insulin sensitivity index ( Matsuda ) decreased from 11.4 ± 3 to 9.9 ± 3.2 ( P = 0.046 ) in group A , but in comparison with other groups , it was not significant . Conclusion : Oral vitamin D had no effect on insulin sensitivity in pre-diabetes patients in 12 weeks treatment . A r and omized double-blind study with a longer duration of treatment is suggested to investigate the effect of vitamin D on insulin resistance AIM To determine the short-term effect of vitamin D(3 ) supplementation on insulin sensitivity in apparently healthy , middle-aged , central ly obese men . SUBJECTS AND METHODS A double-blind r and omized controlled trial was conducted at a tertiary care facility in which 100 male volunteers aged > or = 35 years received three doses of vitamin D(3 ) ( 120,000 IU each ; supplemented group ) fortnightly or placebo ( control group ) . Hepatic fasting insulin sensitivity [ homeostasis model assessment ( HOMA ) , quantitative insulin-sensitivity check index , HOMA-2 ] , postpr and ial insulin sensitivity [ oral glucose insulin sensitivity ( OGIS ) ] , insulin secretion ( HOMA%B , HOMA2-%B ) , lipid profile and blood pressure were measured at baseline and at 6 weeks ' follow-up . RESULTS Seventy-one of the recruited subjects completed the study ( 35 in supplemented group , 36 in control group ) . There was an increase in OGIS with supplementation by per protocol analysis ( P = 0.038 ; intention-to-treat analysis P = 0.055 ) . The age- and baseline 25-hydroxyvitamin D level-adjusted difference in change in OGIS was highly significant ( mean difference 41.1 + /- 15.5 ; P = 0.01 ) . No changes in secondary outcome measures ( insulin secretion , basal indices of insulin sensitivity , blood pressure or lipid profile ) were found with supplementation . CONCLUSION The trial indicates that vitamin D(3 ) supplementation improves postpr and ial insulin sensitivity ( OGIS ) in apparently healthy men likely to have insulin resistance ( central ly obese but non-diabetic ) Background : Vitamin D deficiency is prevalent in diabetes type 2 and this vitamin may be related to insulin action . This r and omized controlled trial study was done to evaluate the effect of vitamin D supplementation on glucose control and insulin resistance in patients with diabetes type 2 . Methods : Participants of this r and omized clinical trial study consisted of 28 patients with type 2 diabetes who received 100 microgram ( 4000 IU ) vitamin D and 30 diabetic patients who received placebo for 2 months between September 2012 and February 2013 . The effect of vitamin D on glucose control was assessed by measuring HbA1c and insulin resistance as HOMA-IR at the baseline and the end of the intervention . Results : The results showed a significant decrease in HbA1c ( from 7.29 ± 0.22 % to 6.76 ± 0.18 % , P<0.001 ) and insulin concentration ( from 8.24 ± 0.97 μIU/mL to 6.55 ± 0.28 μIU/mL , P=0.048 ) , but a non-significant decrease in HOMA-IR  in vitamin D  group . Also , HDL-C level increased significantly in both of vitamin D ( P=0.046 ) and placebo groups ( P=0.028 ) . Conclusion : It seems that vitamin D supplementation has beneficial effects on glucose homeostasis and can increases insulin sensitivity in diabetic 2 patients BACKGROUND Low serum 25-hydroxyvitamin D [ 25(OH)D ] concentrations have been associated with insulin resistance , the metabolic syndrome , and type 2 diabetes . Because many non-Western immigrants in the Netherl and s are vitamin D deficient , obese , and at high risk of diabetes , vitamin D supplementation may contribute to prevent diabetes and insulin resistance . OBJECTIVE We examined the effect of vitamin D supplementation on insulin sensitivity and β cell function in overweight , vitamin D-deficient , non-Western immigrants at high risk of diabetes . DESIGN The study was a 16-wk , r and omized , placebo-controlled trial . A total of 130 non-Western immigrants with prediabetes ( fasting glucose concentration > 5.5 mmol/L or r and om glucose concentration from 7.8 to 11.1 mmol/L ) and vitamin D deficiency ( serum 25[OH]D concentration < 50 nmol/L ) were r and omly assigned after stratification by sex to receive either cholecalciferol ( 1200 IU/d ) or a placebo for 16 wk . All participants received 500 mg Ca/d as calcium carbonate . The primary outcome was the difference in the area under the curve of insulin and glucose after a 75-g oral-glucose-tolerance test after 4 mo of treatment . Secondary outcomes were insulin-sensitivity variables , β cell-function variables , and metabolic syndrome . RESULTS Mean serum 25(OH)D concentrations increased significantly in the vitamin D compared with placebo groups . After 4 mo of therapy , the mean between-group difference was 38 nmol/L ( 95 % CI : 32.1 , 43.9 nmol/L ; P < 0.001 ) . There was no significant effect on insulin sensitivity and β cell function . In a post hoc analysis , when patients with diabetes at baseline were excluded , a significant increase in the insulinogenic index was observed in participants who obtained a 25(OH)D concentration ≥60 nmol/L ( P = 0.040 ) . CONCLUSIONS Vitamin D supplementation in non-Western vitamin D-deficient immigrants with prediabetes did not improve insulin sensitivity or β cell function or change the incidence of metabolic syndrome . However , after the exclusion of diabetic subjects , an improvement in the insulinogenic index was observed in participants who obtained a 25(OH)D concentration ≥60 nmol/L. This trial was registered at trialregister.nl as NTR1827 Background : Vitamin D supplementation has been proposed as a potential strategy to prevent  type 2 diabetes .  Existing clinical trials have been limited by short duration , low doses of vitamin D , variability in participants ' vitamin D-deficiency status , and the use of surrogate measures of body composition , insulin sensitivity , and insulin secretion . Objective : To address existing knowledge gaps , we conducted a double-blind , r and omized , placebo-controlled trial to investigate whether vitamin D supplementation that is provided in a sufficient dose and duration to vitamin D-deficient individuals would improve insulin sensitivity or secretion as measured with the use of gold-st and ard methods . We hypothesized that vitamin D supplementation would improve insulin sensitivity and secretion compared with placebo . Design : Sixty-five overweight or obese , vitamin D-deficient ( 25-hydroxyvitamin D [ 25(OH)D ] concentration ≤50 nmol/L ) adults were r and omly assigned to receive either a bolus oral dose of 100,000 IU cholecalciferol followed by 4000 IU cholecalciferol/d or a matching placebo for 16 wk . Before and after the intervention , participants received gold-st and ard assessment s of body composition ( via dual X-ray absorptiometry ) , insulin sensitivity ( via hyperinsulinemic-euglycemic clamps ) , and insulin secretion [ via intravenous-glucose-tolerance tests ( IVGTTs ) ] . Results : Fifty-four participants completed the study [ 35 men and 19 women ; mean ± SD age : 31.9 ± 8.5 y ; body mass index ( in kg/m2 ) : 30.9 ± 4.4 ] . 25(OH)D increased with vitamin D supplementation compared with placebo ( 57.0 ± 21.3 compared with 1.9 ± 15.1 nmol/L , respectively ; P = 0.02 ) . Vitamin D and placebo groups did not differ in change in insulin sensitivity ( 0.02 ± 2.0 compared with -0.03 ± 2.8 mg · kg-1 · min-1 , respectively ; P = 0.9 ) or first-phase insulin secretion ( -21 ± 212 compared with 24 ± 184 mU/L , respectively ; P = 0.9 ) . Results remained nonsignificant after adjustment for age , sex , percentage of body fat , sun exposure , physical activity , and dietary vitamin D intake ( P > 0.1 ) . Conclusions : Vitamin D supplementation does not improve insulin sensitivity or secretion in vitamin D-deficient , overweight or obese adults , despite using high-dose vitamin D supplementation and robust endpoint measures . Therefore , it is unlikely that vitamin D supplementation would be an effective strategy for reducing diabetes risk even in vitamin D-deficient population s. This trial was registered at clinical trials.gov as NCT02112721 Insulin resistance is one of the most common features of polycystic ovary syndrome ( PCOS ) . Some studies suggest that vitamin D deficiency may have a role in insulin resistance ; thus , the aim of the current study was to determine the effect of vitamin D supplementation on insulin resistance in women with PCOS and a vitamin D deficiency . We hypothesized that vitamin D supplementation would lower the glucose level and insulin resistance in women with PCOS and a vitamin D deficiency . The current study was a r and omized , placebo-controlled , double-blinded trial with 50 women with PCOS and a vitamin D deficiency , 20 to 40 years old , assigned to receive 3 oral treatments consisting of 50,000 IU of vitamin D₃ or a placebo ( 1 every 20 days ) for 2 months ( vitamin D , n = 24 ; placebo , n = 26 ) . The fasting blood glucose , insulin , 25-hydroxyvitamin D , and parathyroid hormone levels , as well as the homeostasis model assessment of insulin resistance and quantitative insulin sensitivity check index were measured at baseline and after treatment . In the vitamin D group , the serum level of 25-hydroxyvitamin D increased ( 6.9 ± 2.8 to 23.4 ± 6.1 ng/mL , P < .0001 ) , and the parathyroid hormone level decreased ( 70.02 ± 43.04 to 50.33 ± 21.99 μ IU/mL , P = .02 ) . There were no significant changes in the placebo group . There was a significant increase in insulin secretion in the vitamin D group ( P = .01 ) , but this was not significant compared with the placebo group . The fasting serum insulin and glucose levels and the insulin sensitivity and homeostasis model assessment of insulin resistance did not change significantly by the end of the study . We were not able to demonstrate the effect of vitamin D supplementation on insulin sensitivity and insulin resistance in women with PCOS and vitamin D deficiency BACKGROUND A suboptimal vitamin D and calcium status has been associated with higher risk of type 2 diabetes in observational studies , but evidence from trials is lacking . OBJECTIVE We determined whether vitamin D supplementation , with or without calcium , improved glucose homeostasis in adults at high risk of diabetes . DESIGN Ninety-two adults were r and omly assigned in a 2-by-2 factorial- design , double-masked , placebo-controlled trial to receive either cholecalciferol ( 2000 IU once daily ) or calcium carbonate ( 400 mg twice daily ) for 16 wk . The primary outcome was the change in pancreatic β cell function as measured by the disposition index after an intravenous-glucose-tolerance test . Other outcomes were acute insulin response , insulin sensitivity , and measures of glycemia . RESULTS Participants had a mean age of 57 y , a body mass index ( BMI ; in kg/m(2 ) ) of 32 , and glycated hemoglobin ( Hb A(1c ) ) of 5.9 % . There was no significant vitamin D × calcium interaction on any outcomes . The disposition index increased in the vitamin D group and decreased in the no-vitamin D group ( adjusted mean change ± SE : 300 ± 130 compared with -126 ± 127 , respectively ; P = 0.011 ) , which was explained by an improvement in insulin secretion ( 62 ± 39 compared with -36 ± 37 mU · L(-1 ) · min , respectively ; P = 0.046 ) . Hb A(1c ) increased less , but nonsignificantly , in the vitamin D group than in the no-vitamin D group ( 0.06 ± 0.03 % compared with 0.14 ± 0.03 % , respectively ; P = 0.081 ) . There was no significant difference in any outcomes with calcium compared with no calcium . CONCLUSION In adults at risk of type 2 diabetes , short-term supplementation with cholecalciferol improved β cell function and had a marginal effect on attenuating the rise in Hb A(1c ) . This trial was registered at clinical trials.gov as NCT00436475 Background & objectives : Patients with diabetes and vitamin-D insufficiency have increased insulin resistance . Similar observations among individuals with prediabetes are not well documented . The aim of this study was to find the occurrence of vitamin-D insufficiency/deficiency among individuals with prediabetes and to evaluate the relationship between vitamin-D status and insulin resistance . Methods : One hundred fifty seven individuals with prediabetes who fulfilled all the inclusion and exclusion criteria underwent clinical examination , anthropometric measurements ( waist circumference , waist-hip ratio , waist-height ratio ) and blood sampling after overnight fast for estimation of fasting blood glucose , fasting insulin , 25(OH)vitamin-D , intact parathyroid hormone ( iPTH ) and lipid profile . One hour post 75 g glucose ( 1hPG ) blood glucose during oral glucose tolerance test was measured . Results : Vitamin-D deficiency/insufficiency was found in 115 ( 73.25 % ) individuals with prediabetes .  Severe vitamin-D deficiency ( < 10 ng/ml ) was seen in 14.65 per cent individuals . Individuals with the lowest vitamin-D levels ( < 10 ng/ml ) had the highest insulin resistance ( HOMA2-IR : 2.04 ± 0.67 ) . Serum 25(OH)D had a statistically significant inverse correlation with insulin resistance ( HOMA2-IR ; r=-0.33 ; P=0.008 ) , and positive correlation with insulin sensitivity ( QUICKI ; r=0.39 ; P=0.002 ) , after adjusting for BMI and HbA1c . There was no correlation between vitamin-D status and estimated beta cell mass ( HOMA-β ) . The mean waist-height ratio among individuals with prediabetes was 0.57 ( normal<0.5 ) indicating a high risk of cardiovascular morbidity . Individuals with elevated 1hPG>155 mg/dl had significantly higher BMI and worse insulin resistance , and 1hPG correlated well with 2 hour post glucose blood glucose ( r=0.57 ; P<0.001 ) . Interpretations & conclusions : Vitamin-D deficiency/insufficiency may have some role in the development/worsening of insulin resistance in individuals with prediabetes in our country who have a high cardiovascular risk . Prospect i ve studies on a large group of individuals need to be done to confirm the findings Vitamin D has been shown to increase insulin release from pancreatic islet cells in vitro , and to improve insulin secretion in vitamin D-deficient animals . Few attempts have been made to evaluate this issue directly in humans . We studied 35 otherwise healthy diabetic subjects in the early spring at the seasonal nadir of 25-hydroxyvitamin D [ 25(OH)D ] concentrations ( mean 35 + /- 7 nmol/L ) .  Fasting glucose , insulin , C-peptide , and glucagon concentrations , and their responses to Sustacal stimulation were not related to indexes of mineral metabolism . In 20 subjects , a double-blinded , placebo-controlled , crossover trials of 1,25-dihydroxyvitamin D[1,25](OH)2D ] treatment ( 1 micrograms/d for 4 d ) had no effect on fasting or stimulated glucose , insulin , C-peptide , or glucagon concentrations . However , insulin and C-peptide responses to Sustacal after 1,25(OH)2D treatment were related to duration of diabetes ( r2 = 0.28 , P = 0.052 and r2 = 0.25 , P = 0.002 , respectively ) in that short duration correlated with improvement after 1,25(OH)2D treatment . Hence , vitamin D nutrition , or 1,25(OH)2D therapy , had no major effect on glucose homeostasis in non-insulin-dependent diabetes mellitus CONTEXT Vitamin D deficiency is associated with insulin resistance and risk of future diabetes . OBJECTIVE The objective of the study was to test whether supplementation with vitamin D to subjects with prediabetes will prevent progression to type 2 diabetes mellitus ( T2DM ) . DESIGN This was a r and omized controlled trial performed in 2008 through 2015 . SETTING The study was conducted at the clinical research unit at a teaching hospital . PATIENTS Five hundred eleven subjects ( mean age 62 y , 314 males ) with prediabetes diagnosed with an oral glucose tolerance test as part of the Tromsø Study 2007–2008 were included . A total of 256 were r and omized to vitamin D and 255 to placebo .  Twenty-nine subjects in the vitamin D and 24 in the placebo group withdrew because of adverse events . INTERVENTIONS Interventions included vitamin D ( cholecalciferol ) 20 000 IU/wk vs placebo for 5 years . Annual oral glucose tolerance tests were performed . MAIN OUTCOME MEASURE Progression to T2DM was the main outcome measure . Secondary outcomes were change in glucose levels , insulin resistance , serum lipids , and blood pressure . RESULTS The mean baseline serum 25-hydroxyvitamin D level was 60 nmol/L ( 24 ng/mL ) . One hundred three in the vitamin D and 112 in the placebo group developed T2DM ( hazard risk 0.90 ; 95 % confidence interval 0.69–1.18 , Cox regression , P = .45 , intention to treat analysis ) . No consistent significant effects on the other outcomes were seen . Subgroup analyses in subjects with low baseline 25-hydroxyvitamin D yielded similar results . No serious side effects related to the intervention were recorded . CONCLUSIONS In subjects without vitamin D deficiency , vitamin D supplementation is unlikely to prevent progression from prediabetes to diabetes . Very large studies with inclusion of vitamin D-deficient subjects will probably be needed to show such a putative effect . This study tested if supplementation with  vitamin D to subjects with prediabetes will prevent progression to type 2 diabetes ( T2DM ) Background & the purpose of the study Prevalence of type 2 diabetes mellitus ( T2DM ) is increasing worldwide . To reduce its risk and progression , preventive strategies are needed . Vitamin supplementation such as vitamin D is one of the strategies . This study was design ed to investigate the effect of injection of vitamin D on insulin resistance and anthropometric parameters in T2DM . Methods This r and omized double-blind clinical trial was conducted with 42 diabetic patients in two groups ; intervention group with  single intramuscular injection of 300,000 International Unit ( IU ) of vitamin D3 and the placebo group . After recording demographic and anthropometric factors ( waist circumference , blood pressure and body mass index ) , fasting blood sample s was taken for measurement of blood glucose , 25-hydroxyvitamin D3 ( 25-OHD3 ) , insulin , glycosylated hemoglobin A1c ( HbA1c ) and estimation of Homeostasis Model Assessment Index ( HOMA ) in two times ; before study and after three months . Results Two groups had similar baseline characteristics ( each group = 21 subjects ) . Three months after vitamin D injection , HbA1c , anthropometric factors and HOMA index in intervention group stayed constant , however , serum 25- OHD3 was significantly increased ( p = 0.007 ) . Conclusion The present data is not convincing and further studies with large sample sizes are needed to show the definite effect of injection of vitamin D on control of diabetes and its risk AIMS Vitamin D deficiency may increase the risk for type 2 diabetes . African Americans tend to have poor vitamin D status and increased risk of diabetes , but effects of vitamin D supplementation on components of diabetes risk have not been tested in this group . This study was conducted to determine whether vitamin D supplementation improves insulin secretion , insulin sensitivity and glycaemia in African Americans with prediabetes or early diabetes . METHODS In this r and omized , placebo-controlled trial , we examined the effect of 4000 IU/day vitamin D(3 , ) on glycaemia and contributing measures including insulin secretion , insulin sensitivity and the disposition index over 12 weeks in 89 overweight or obese African Americans with prediabetes or early diabetes . Outcome measures were derived from oral glucose tolerance testing . RESULTS Mean plasma 25-hydroxyvitamin D was about 40 nmol/l in the placebo and vitamin D groups at baseline and increased to 81 nmol/l with supplementation . Insulin sensitivity decreased by 4 % in the vitamin D group compared with a 12 % increase in the placebo group ( p = 0.034 ) . Insulin secretion increased by 12 % in the vitamin D group compared with a 2 % increase in the placebo group ( p = 0.024 ) , but changes in the disposition index were similar across groups . There was no effect of supplementation on post-load glucose or other measures of glycaemia . CONCLUSIONS Supplementation with 4000 IU/day vitamin D(3 ) successfully corrected vitamin D insufficiency and had divergent effects on insulin secretion and sensitivity with no overall effect on disposition index or glycaemia . In this study , vitamin D supplementation for 3 months did not change the pathophysiology of prediabetes in overweight and obese African Americans
Conclusions Short-term ( 4–12 weeks ) supplementation with vitamin D is associated with lower fasting glucose levels in ESRD with no change in fasting insulin levels .
Abstract Purpose We tested whether short-term vitamin D supplementation improves insulin resistance in patients with kidney disease , a condition with little intrinsic vitamin D activity .