Effect of vitamin D supplementation on glycemic control in patients with type 2 diabetes: a systematic review of interventional studies Effect of Vitamin D Supplementation on Glucose Control and Inflammatory Response in Type II Diabetes: A Double Blind, Randomized Clinical Trial Serum 25(OH)D and Type 2 Diabetes Association in a General Population Baseline Characteristics of the Vitamin D and Type 2 Diabetes (D2d) Study: A Contemporary Prediabetes Cohort That Will Inform Diabetes Prevention Efforts A randomized, placebo-controlled trial of vitamin D supplementation to improve glycaemia in overweight and obese African Americans. Association of vitamin D deficiency with incidence of type 2 diabetes in high-risk Asian subjects. Vitamin D improves endothelial function in patients with Type 2 diabetes mellitus and low vitamin D levels. Vitamin D supplementation in obese type 2 diabetes subjects in Ajman, UAE: a randomized controlled double-blinded clinical trial Associations between Vitamin D Status and Type 2 Diabetes Measures among Inuit in Greenland May Be Affected by Other Factors Vitamin D supplementation for the prevention of type 2 diabetes in overweight adults: study protocol for a randomized controlled trial Study protocol: a randomised placebo-controlled clinical trial to study the effect of vitamin D supplementation on glycaemic control in type 2 Diabetes Mellitus SUNNY trial The Effects of Vitamin D Supplementation on Glucose Control and Insulin Resistance in Patients with Diabetes Type 2: A Randomized Clinical Trial Study Vitamin D and incidence of diabetes: a prospective cohort study. Role of Vitamin D in Insulin Secretion and Insulin Sensitivity for Glucose Homeostasis 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 Lack of effect of subtherapeutic vitamin D treatment on glycemic and lipid parameters in Type 2 diabetes: A pilot prospective randomized trial.
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 : Diabetes mellitus ( DM ) and vitamin D deficiency are major health concerns around the world . Evidence suggests a possible role of vitamin D in improvement of insulin secretion and sensitivity . Objectives : We assessed whether vitamin D supplementation could be used in vitamin D deficient-type II diabetes to improve glucose metabolism , components of metabolic syndrome ( MetS ) and specific inflammatory biomarkers . Patients and Methods : A double blind , r and omized clinical trial was conducted in King Khalid University Hospital , Saudi Arabia to evaluate the effect of cholecalciferol supplementation on glycemic control , MetS components and specific inflammatory biomarkers including tumor necrosis factor-alpha ( TNF-α ) , Interleukin ( IL-6 ) , leptin , adiponectin and vascular cell adhesion molecule-1 ( VCAM-1 ) . Twenty-two patients with type II diabetes with insulin resistance , glycated hemoglobin ( HbA1c ) ≥ 6 ( 42 mmol/mol ) and serum 25(OH)D < 50 nmol/L were r and omized using a computer program to receive either supplementation with cholecalciferol ( 5000 IU/day ) or placebo for 12 weeks . The primary outcome was change in HbA1c levels from baseline . Results : Median [ IQR ] 25(OH)D levels increased significantly in the vitamin D group as 58.1 [ 48 , 67.3 ] nmol/L ( P = 0.002 ) . There was no significant difference in the change of HbA1c between the groups ( P = 0.5 ) with a decrease of -0.1 % [ -1 , 0.5 ] in the vitamin D group and an increase of 0.15 % [ 0.1 , 0.2 ] in the placebo group . A significant improvement was observed in the homeostasis model of assessment of β-cell activity ( HOMA-%B ) ( P = 0.03 ) with vitamin D supplementation compared to baseline . Conclusions : Vitamin D repletion for 12 weeks increased serum vitamin D concentrations and improved β-cell activity in vitamin D-deficient type II diabetes with no significant changes in HbA1c or insulin sensitivity OBJECTIVE This study aim ed to examine vitamin D status as a determinant for development of type 2 diabetes and deterioration of glucose homeostasis . RESEARCH DESIGN AND METHODS A r and om sample of the general population of Copenhagen , Denmark , was taken as part of the Inter99 study . Included were 6,405 men and women aged 30–65 years at baseline ( 1999–2001 ) , with 4,296 participating in the follow-up examination 5 years later ( 2004–2006 ) .  Vitamin D was determined at baseline as serum 25-hydroxyvitamin D [ 25(OH)D ] . Diabetes was defined based on an oral glucose tolerance test and a glycosylated hemoglobin ( HbA1c ) test . Secondary outcomes included continuous markers of glucose homeostasis . RESULTS The risk of incident diabetes associated with a 10 nmol/L increase in 25(OH)D was odds ratio ( OR ) 0.91 ( 95 % CI 0.84–0.97 ) in crude analyses . The association became statistically nonsignificant after adjustment for confounders , with an OR per 10 nmol/L of 0.94 ( 0.86–1.03 ) . Low 25(OH)D status was significantly associated with unfavorable longitudinal changes in continuous markers of glucose homeostasis after adjustment for confounders . Fasting and 2-h glucose and insulin as well as the degree of insulin resistance increased significantly more during follow-up among those with low 25(OH)D levels compared with those with higher levels . CONCLUSIONS Low 25(OH)D status was not significantly associated with incident diabetes after adjustment for confounders . However , it was significantly associated with unfavorable longitudinal changes in continuous markers of glucose homeostasis , indicating that low vitamin D status could be related to deterioration of glucose homeostasis OBJECTIVE To describe baseline characteristics of the Vitamin D and Type 2 Diabetes ( D2d ) study , the first large U.S. diabetes prevention clinical trial to apply current American Diabetes Association ( ADA ) criteria for prediabetes . RESEARCH DESIGN AND METHODS This is a multicenter ( n = 22 sites ) , r and omized , double-blind , placebo-controlled , primary prevention clinical trial testing effects of oral daily 4,000 IU cholecalciferol ( D3 ) compared with placebo on incident diabetes in U.S. adults at risk for diabetes . Eligible participants were at risk for diabetes , defined as not meeting criteria for diabetes but meeting at least two 2010 ADA glycemic criteria for prediabetes : fasting plasma glucose ( FPG ) 100–125 mg/dL , 2-h postload glucose ( 2hPG ) after a 75-g oral glucose load 140–199 mg/dL , and /or a hemoglobin A1c ( HbA1c ) 5.7–6.4 % ( 39–46 mmol/mol ) . RESULTS A total of 2,423 participants ( 45 % of whom were women and 33 % nonwhite ) were r and omized to cholecalciferol or placebo . Mean ( SD ) age was 60 ( 9.9 ) years and BMI 32.1 ( 4.5 ) kg/m2 . Thirty-five percent met all three prediabetes criteria , 49 % met the FPG/HbA1c criteria only , 9.5 % met the 2hPG/FPG criteria only , and 6.3 % met the 2hPG/HbA1c criteria only . Black participants had the highest mean HbA1c and lowest FPG concentration compared with white , Asian , and other races ( P < 0.01 ) ; 2hPG concentration did not differ among racial groups . When compared with previous prediabetes cohorts , the D2d cohort had lower mean 2hPG concentration but similar HbA1c and FPG concentrations . CONCLUSIONS D2d will establish whether vitamin D supplementation lowers risk of diabetes and will inform about the natural history of prediabetes per contemporary ADA criteria 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 BACKGROUND Recent studies suggest an association between 25-hydroxyvitamin D [ 25(OH)D ] and type 2 diabetes ( T2D ) risk . However , prospect i ve studies investigating the relation between vitamin D inadequacy and incidence of T2D incorporating obesity and dynamic measures of insulin resistance ( IR ) and pancreatic β cell function are limited . OBJECTIVE We tested the hypothesis that baseline 25(OH)D is associated with the incidence of T2D in high-risk subjects for up to 5 y of follow-up , independently of obesity , baseline IR , and β cell function . DESIGN We recruited 1080 nondiabetic Korean subjects [ mean ± SD age : 49.5 ± 11.4 y ] based on the presence of one or more risk factors for T2D , including obesity , hypertension , dyslipidemia , and /or family history of T2D . We measured anthropometric and biochemical indicators , HOMA2-IR , and the insulinogenic index ( IGI ; calculated as change in insulin at 30 min/change in glucose at 30 min ) from a 75-g oral-glucose-tolerance test . RESULTS Of the participants , 10.5 % had a serum 25(OH)D deficiency ( < 10 ng/mL ) , 51.6 % had an insufficiency ( 10.0 - 19.9 ng/mL ) , and 38.0 % had a sufficiency ( ≥20 ng/mL ) , and the incidence of T2D at 32.3 ± 15.6 mo ( ±SD ) declined accordingly : 15.9 % , 10.2 % , and 5.4 % , respectively ( P < 0.001 ) . After adjustment for age , sex , blood pressure , lifestyles , family history , season , parathyroid hormone , and high-sensitivity C-reactive protein , the participants with 25(OH)D deficiency had an increased risk of T2D independently of BMI , HOMA2-IR , and IGI ; the HRs were 2.06 ( 95 % CI : 1.22 , 3.49 ) for 25(OH)D 10 - 19.9 ng/mL compared with ≥20 ng/mL and 3.23 ( 95 % CI : 1.66 , 6.30 ) for 25(OH)D < 10 ng/mL compared with ≥20 ng/mL. CONCLUSION The current prospect i ve study suggests that vitamin D metabolism may play a role in T2D pathogenesis independently of known risk factors . This trial was registered at clinical trials.gov as NCT01508481 AIMS To test whether a single large dose of vitamin D2 can improve endothelial function in patients with Type 2 diabetes mellitus and low serum 25-hydroxyvitamin D levels . METHODS Double-blind , parallel group , placebo-controlled r and omized trial . A single dose of 100,000 IU vitamin D2 or placebo was administered to patients with Type 2 diabetes over the winter , when levels of circulating 25-hydroxyvitamin D were likely to be lowest . Patients were enrolled if their baseline 25-hydroxyvitamin D level was < 50 nmol/l .  Endothelial function and blood pressure were measured and fasting blood sample s were taken at baseline and 8 weeks after administration of vitamin D. RESULTS Forty-nine per cent of subjects screened had 25-hydroxyvitamin D levels < 50 nmol/l . Thirty-four subjects completed the study , with a mean age of 64 years and a baseline 25-hydroxyvitamin D level of 38.3 nmol/l .  Vitamin D supplementation  increased 25-hydroxyvitamin D levels by 15.3 nmol/l relative to placebo and significantly improved flow mediated vasodilatation ( FMD ) of the brachial artery by 2.3 % . The improvement in FMD remained significant after adjusting for changes in blood pressure .  Vitamin D supplementation significantly decreased systolic blood pressure by 14 mmHg compared with placebo ; this did not correlate with change in FMD . CONCLUSIONS Vitamin D insufficiency is common in patients with Type 2 diabetes during winter in Scotl and . A single large dose of oral vitamin D2 improves endothelial function in patients with Type 2 diabetes and vitamin D insufficiency Objectives : To study the effect of Vitamin D3 supplementation on metabolic control in an obese type 2 diabetes Emirati population . Methods : This r and omized double-blind clinical trial was conducted with 87 vitamin D-deficient obese , type 2 diabetic participants . The vitamin D-group ( n=45 ) and the placebo group ( n=42 ) were matched for gender , age , HbA1c and 25-hydroxy vitamin D ( 25(OH ) D ) at the baseline . The study was divided into two phases of 3 months each ; in phase 1 , the vitamin D-group received 6000 IU vitamin D3/day followed by 3000 IU vitamin D3/day in phase 2 , whereas the placebo group ( n=42 ) received matching placebo . Results : After supplementation , serum 25(OH ) D peaked in the vitamin D-group in phase 1 ( 77.2±30.1 nmol/l , P=0.003 ) followed by a decrease in the phase 2 ( 61.4±18.8 nmol/l , P=0.006 ) , although this was higher compared with baseline . In the placebo group , no difference was observed in the serum 25(OH ) D levels throughout the intervention . Relative to baseline serum , parathyroid hormone decreased 24 % ( P=0.003 ) in the vitamin D-group in phase 2 , but remained unchanged in the placebo group . No significant changes were observed in blood pressure , fasting blood glucose , HbA1c , C-peptide , creatinine , phosphorous , alkaline phosphatase , lipids , C-reactive protein or thyroid stimulating hormone concentrations compared with baseline in either group . Conclusions : Six months of vitamin D3 supplementation to vitamin D-deficient obese type 2 diabetes patients in the UAE normalized the vitamin D status and reduced the incidence of eucalcemic parathyroid hormone elevation but showed no effect on the metabolic control Objective Epidemiological studies have provided evidence of an association between vitamin D insufficiency and  type 2 diabetes .  Vitamin D levels have decreased among Inuit in Greenl and , and type 2 diabetes is increasing . We hypothesized that the decline in vitamin D could have contributed to the increase in type 2 diabetes , and therefore investigated associations between serum 25(OH)D3 as a measure of vitamin D status and glucose homeostasis and glucose intolerance in an adult Inuit population . Methods 2877 Inuit ( ≥18 years ) r and omly selected for participation in the Inuit Health in Transition study were included .  Fasting- and 2hour plasma glucose and insulin , C-peptide and HbA1c  were measured , and associations with serum 25(OH)D3 were analysed using linear and logistic regression . A sub sample of 330 individuals who also donated a blood sample in 1987 , were furthermore included . Results After adjustment , increasing serum 25(OH)D3 ( per 10 nmol/L ) was associated with higher fasting plasma glucose ( 0.02 mmol/L , p = 0.004 ) , 2hour plasma glucose ( 0.05 nmol/L , p = 0.002 ) and HbA1c ( 0.39 % , p<0.001 ) , and with lower beta-cell function ( -1.00 mmol/L , p<0.001 ) . Serum 25(OH)D3 was positively associated with impaired fasting glycaemia ( OR : 1.08 , p = 0.001 ) , but not with IGT or type 2 diabetes . Conclusions Our results did not support an association between low vitamin D levels and risk of type 2 diabetes . Instead , we found weak positive associations  between vitamin D levels and fasting- and 2hour plasma glucose levels , HbA1c and impaired fasting glycaemia , and a negative association with beta-cell function , underlining the need for determination of the causal relationship Background Despite Australia ’s sunny climate , low vitamin D levels are increasingly prevalent . Sun exposure is limited by long working hours , an increase in time spent indoors , and sun protection practice s , and there is limited dietary vitamin D fortification . While the importance of vitamin D for bone mineralization is well known , its role as a protective agent against chronic diseases , such as type 2 diabetes and cardiovascular disease , is less understood . Observational and limited intervention studies suggest that vitamin D might improve insulin sensitivity and secretion , mainly via its anti-inflammatory properties , thereby decreasing the risk of development and progression of type 2 diabetes . The primary aim of this trial is to investigate whether improved plasma concentrations of 25-hydroxyvitamin D ( 25(OH)D ) , obtained through vitamin D supplementation , will increase insulin sensitivity and insulin secretion . A secondary aim is to determine whether these relationships are mediated by a reduction in underlying sub clinical inflammation associated with obesity . Methods / Design Fifty overweight but otherwise healthy nondiabetic adults between 18 and 60 years old , with low vitamin D levels ( 25(OH)D < 50 nmol/l ) , will be r and omly assigned to intervention or placebo . At baseline , participants will undergo a medical review and anthropometric measurements , including dual X-ray absorptiometry , an intravenous glucose tolerance test , muscle and fat biopsies , a hyperinsulinemic euglycemic clamp  , and question naires assessing diet , physical activity , sun exposure , back and knee pain , and depression . The intervention group will receive a first dose of 100,000 IU followed by 4,000 IU vitamin D ( cholecalciferol ) daily , while the placebo group will receive apparently identical capsules , both for a period of 16 weeks . All measurements will be repeated at follow-up , with the primary outcome measure expressed as a change from baseline in insulin sensitivity and secretion for the intervention group compared with the placebo group . Secondary outcome measures will compare changes in anthropometry , cardiovascular risk factors , and inflammatory markers . Discussion The trial will provide much needed clinical evidence on the impact of vitamin D supplementation on insulin resistance and secretion and its underlying mechanisms , which are relevant for the prevention and management of type 2 diabetes . Trial registration Clinical trials.gov ID : NCT02112721 Background Besides the classical role of vitamin D on calcium and bone homeostasis , vitamin D deficiency has recently been identified as a contributing factor in the onset of insulin resistance in type 2 diabetes mellitus . However , it is uncertain whether vitamin D deficiency and poor glycaemic control are causally interrelated or that they constitute two independent features of type 2 diabetes mellitus . There are limited clinical trials carried out which measured the effect of vitamin D supplementation on glycaemic control . The objective of this study is to investigate the effect of vitamin D supplementation on glycaemic control and quality of life in patients with type 2 diabetes mellitus . Methods / design In a r and omised double-blind placebo-controlled trial conducted in five general practice s in the Netherl and s three hundred patients with type 2 diabetes mellitus treated with lifestyle advises or metformin or sulphonylurea-derivatives are r and omised to receive either placebo or 50,000 IU Vitamin D3 at monthly intervals . The primary outcome measure is the change in glycated haemoglobin level between baseline and six months . Secondary outcome measures include blood pressure , anthropometric parameters , lipid profile , insulin resistance , quality of life , advanced glycation end products and safety profiles . Quality of life will be measured by The Short Form ( SF-36 ) Health Survey question naire . Advanced glycation end products are measured by an AGE-reader . Discussion This trial will be the first study exploring the effect of vitamin D supplementation on both glycaemic control and quality of life in patients with type 2 diabetes mellitus . Our findings will contribute to the knowledge of the relationship between vitamin D status and insulin resistance in patients with type 2 diabetes mellitus . Trial registration The Netherl and s trial register : 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 & AIMS To investigate the relationship between levels of 25-hydroxyvitamin D and the  incidence of type 2 diabetes in a Spanish population . METHODS We undertook a population -based prospect i ve study in a population from southern Spain . The first phase of the study ( 1996 - 1998 ) included 1226 individuals . Of this original cohort , 988 persons were reassessed in 2002 - 2004 and 961 in 2005 - 2007 . Measurements were made of  25-hydroxyvitamin D and intact parathyroid hormone  in 2002 - 2004 and an  oral glucose tolerance test  was done in three time points . RESULTS The incidence of diabetes in subjects with 25-hydroxyvitamin D levels ≤ 18.5 ng/mL ( percentile 25 ) was 12.4 % vs 4.7 % in subjects with levels > 18.5 ng/mL. The likelihood of having diabetes during the four years of follow-up was significantly lower in the subjects with higher levels of 25-hydroxyvitamin D [ OR = 0.17 ( 0.05 - 0.61 ) ] . None of the subjects with levels higher than 30 ng/mL developed diabetes . CONCLUSION In this prospect i ve study , we found a significant inverse association between serum 25-hydroxyvitamin D levels and the risk for type 2 diabetes in a population from the south of Spain Vitamin D functions are not limited to skeletal health benefits and may extend to preservation of insulin secretion and insulin sensitivity . This review summarizes the literature related to potential vitamin D influences on glucose homeostasis and insulin sensitivity . Cross-sectional data provide some evidence that circulating 25-hydroxyvitamin D ( 25(OH)D ) is inversely associated with insulin resistance , although direct measurements of insulin sensitivity are required for confirmation . Reported associations with insulin secretion , however , are contradictory . Available prospect i ve studies support a protective influence of high 25(OH)D concentrations on type 2 diabetes mellitus risk . There is a general lack of consistency in vitamin D intervention outcomes on insulin secretion and sensitivity , likely due to differences in subject population s , length of interventions , and forms of vitamin D supplementation . Vitamin D receptor gene polymorphisms and vitamin D interactions with the insulin like growth factor system may further influence glucose homeostasis . The ambiguity of optimal vitamin D dosing regimens and optimal therapeutic concentrations of serum 25(OH)D limit available intervention studies . Future studies , including cross-sectional and prospect i ve , should be performed in population s at high risk for both vitamin D deficiency and type 2 diabetes mellitus . Well- design ed , placebo-controlled , r and omized intervention studies are required to establish a true protective influence of  vitamin D on glucose homeostasis 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 BACKGROUND Epidemiological studies suggest a higher prevalence of metabolic syndrome and its components among individuals with vitamin D deficiency . The aim of the present study was to determine whether vitamin D treatment  improves glucose control and insulin sensitivity in Type 2 diabetes mellitus ( T2DM ) . METHODS Subjects with T2DM and serum 25-hydroxyvitamin D ( 25(OH)D ) concentrations < 25 ng/mL were r and omized to receive 400 IU ( Group 1 ) or 1200 IU ( Group 2 ) cholecalciferol for 4 months . Fasting plasma glucose , glycosylated hemoglobin ( HbA1c ) , Quantitative Insulin Sensitivity Check Index ( QUICKI ) , serum lipid levels and serum adiponectin were measured at baseline and at 4 months . RESULTS Mean 25(OH)D levels increased in both groups ( from 17.6±1.5 to 25.5±1.8 ng/mL in Group 1 and from 15.6±1.4 to 27.4±2.4 ng/mL in Group 2 ; P≤0.001 vs baseline for each group ) . No significant differences were noted in fasting plasma glucose , HbA1c , QUICKI , serum adiponectin , and lipid levels compared with baseline within groups or between the two groups . CONCLUSIONS In the present pilot study , conventional vitamin D treatment at a level improving , but not optimizing , serum 25(OH)D did not improve glycemia , insulin sensitivity , or lipid profile . However , diabetes and lipids were relatively well controlled at baseline . Future studies should be design ed to achieve optimal concentrations of serum 25(OH)D ( at least > 32 ng/mL ) and should include subjects showing more abnormal parameters of glycemia , lipid , and insulin sensitivity at baseline
This meta- analysis concludes that hypovitaminosis D is associated with increased risk of hyperglycemia both in diabetic and non-diabetic subjects .
There is evidence that vitamin D status is associated with type 2 diabetes .
Many observational studies have been performed investigating the relationship of vitamin D status and circulating biomarkers of glycemic regulation .
To find out whether this association holds , we conducted a systematic review and meta- analysis of cross sectional and longitudinal studies .