title: Prevalence of vitamin D deficiency and its correlates: results of a community-based study conducted in Karachi, Pakistan Predicted 25-hydroxyvitamin D score and change in fasting plasma glucose in the Framingham offspring study Serum 25(OH)D and Type 2 Diabetes Association in a General Population Vitamin D, glucose tolerance and insulinaemia in elderly men Decreased Serum Concentrations of 25-Hydroxycholecalciferol Are Associated With Increased Risk of Progression to Impaired Fasting Glucose and Diabetes Serum vitamin-D predicts insulin resistance in individuals with prediabetes Associations between Vitamin D Status and Type 2 Diabetes Measures among Inuit in Greenland May Be Affected by Other Factors Vitamin D, Insulin Secretion, Sensitivity, and Lipids Plasma vitamin D is associated with fasting insulin and homeostatic model assessment of insulin resistance in young adult males, but not females, of the Jerusalem Perinatal Study. Plasma 25-hydroxyvitamin D and its genetic determinants in relation to incident type 2 diabetes: a prospective case-cohort study Serum 25-hydroxyvitamin D level and diabetic nephropathy in patients with type 2 diabetes mellitus 25-Hydroxyvitamin D [25(OH)D] levels and diabetic foot ulcer: is there any relationship? Relationship between glycated hemoglobin and circulating 25-hydroxyvitamin D concentration in African American and Caucasian American men. A genome-wide methylation study of severe vitamin D deficiency in African American adolescents. Vitamin D and incidence of diabetes: a prospective cohort study. A global representation of vitamin D status in healthy populations
abstract: Summary Of the 305 premenopausal females in a cross-sectional study in r and omly selected communities of Karachi , Pakistan , 90.1 % showed to be vitamin D deficient . Age , town of residence , and housing structure were significant predictors of vitamin D levels . Measures to address D deficiency and its associated long latency effects are urgently needed . Aims This study aims to find out the prevalence and risk factors of vitamin D deficiency in community-dwelling premenopausal females in Karachi . Methods A cross-sectional study was conducted in r and omly selected communities downtown ( Saddar ) and suburbs ( Gulshan and Malir Town ) in Karachi , Pakistan . Information related to sociodemographics ( age , education , employment , and household income ) , housing structure , sunlight exposure , and skin pigmentation as well as dietary intake ( using a food frequency question naire ) was collected . Serum vitamins D3 levels were also measured . Mean and SD was computed for continuous variables and frequency and proportions were computed for categorical variables . Data were further analyzed by Chi-square test and ANOVA . Multiple linear regression analysis was done to find out determinants of vitamin D ( VD ) levels . Results Total of 305 premenopausal females were recruited .  Mean age , BMI , and waist circumference of the study participants was 31.97 ± 8 years , 25.06 ± 5.6 kg/m2 , and 88.42 ± 13.3 cm , respectively . Majority of the females were vitamin D deficient ( 91.50 % ) with mean vitamin D levels of 21.77 ± 21.66 nm/L. Mean vitamin D levels were significantly different among females residing in downtown and suburbs . High frequency of vitamin D deficiency was observed in females dwelling in downtown ( Saddar ) . According to the results of multiple linear regression analysis , determinants of VD levels were age , town of residence , and housing structure . Conclusion High prevalence of vitamin D deficiency is seen in females in the community of Karachi , Pakistan . Age , town of residence , and housing structure were the significant predictors of vitamin D levels . Measures to combat the issue of D deficiency and its associated long latency effects are urgently needed Data on the association between vitamin D status and actual change in glycemic measures are limited . We examined the prospect i ve association between a predicted 25-hydroxyvitamin D ( 25(OH)D ) score and change in fasting plasma glucose concentration over a mean follow-up of 7 years , in 2571 men and women ( mean age 54 years ) without diabetes in the Framingham Offspring Study cohort . After adjustment for age , sex , body mass index and fasting plasma glucose at baseline , higher predicted 25(OH)D score at baseline was associated with a smaller 7-year increase in fasting plasma glucose concentrations ( 0.23 mmol/l versus 0.35 mmol/l for highest versus lowest tertile of 25(OH)D score , respectively , P-trend=0.002 ) . Vitamin D status may be an important determinant for change in fasting plasma glucose concentration among middle-aged and older adults without diabetes 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 Summary  Vitamin D status  was assessed in 142 elderly Dutchmen participating in a prospect i ve population -based study of environmental factors in the aetiology of non-insulin-dependent diabetes mellitus . Of the men aged 70–88 years examined between March and May 1990 , 39 % were vitamin D depleted . After adjustment for confounding by age , BMI , physical activity , month of sampling , cigarette smoking and alcohol intake the 1-h glucose and area under the glucose curve during a st and ard 75-g oral glucose tolerance test ( OGTT ) were inversely associated with the serum concentration of 25-OH vitamin D ( r = −0.23 , p < 0.01 ; r = −0.26 , p < 0.01 , respectively ) . After excluding newly diagnosed diabetic patients total insulin concentrations during OGTT were also inversely associated with the concentration of 25-OH vitamin D ( r = −0.18 to −0.23 , p < 0.05 ) . Hypovitaminosis D may be a significant risk factor for glucose intolerance . [ Diabetologia ( 1997 ) 40 : 344–347 OBJECTIVE To study the association between vitamin D status and the risk of incident impaired fasting glucose ( IFG ) and diabetes  in a population -based cohort of diabetes-free subjects . RESEARCH DESIGN AND METHODS In a historical prospect i ve cohort study of subjects from the Clalit Health Services data base , which includes information on nearly 4 million people , diabetes-free subjects aged 40–70 years with serum 25-hydroxycholecalciferol ( 25-OHD ) measurements available were followed for 2 years to assess the development of IFG and diabetes in five 25-OHD subgroups : ≥25 , 25.1–37.5 , 37.6–50 , 50.1–75 , and > 75 nmol/L. RESULTS The baseline cohort included 117,960 adults : 83,526 normoglycemic subjects and 34,434 subjects with IFG . During follow-up , 8,629 subjects ( 10.3 % of the normoglycemic group ) developed IFG , and 2,162 subjects ( 1.8 % of the total cohort ) progressed to diabetes . A multivariable model adjusted for age , sex , population group , immigrant status , BMI , season of vitamin D measurement , LDL and HDL cholesterol , triglycerides , estimated glomerular filtration rate , history of hypertension or cardiovascular disease , Charlson comorbidity index , smoking , and socioeconomic status revealed an inverse association between 25-OHD and the risk of progression to IFG and diabetes . The odds of transitioning from normoglycemia to IFG , from normoglycemia to diabetes , and from IFG to diabetes in subjects with a 25-OHD level ≤25 nmol/L were greater than those of subjects with a 25-OHD level > 75 nmol/L [ odds ratio 1.13 ( 95 % CI 1.03–1.24 ) , 1.77 ( 1.11–2.83 ) , and 1.43 ( 1.16–1.76 ) , respectively ] . CONCLUSIONS Vitamin D deficiency appears to be an independent risk factor for the development of IFG and diabetes 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 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 OBJECTIVE Vitamin D deficiency is associated with an unfavorable metabolic profile in observational studies . The intention was to compare insulin sensitivity ( the primary end point ) and secretion and lipids in subjects with low and high serum 25(OH)D ( 25-hydroxyvitamin D ) levels and to assess the effect of vitamin D supplementation on the same outcomes among the participants with low serum 25(OH)D levels . RESEARCH DESIGN AND METHODS Participants were recruited from a population -based study ( the Tromsø Study ) based on their serum 25(OH)D measurements . A 3-h hyperglycemic clamp was performed , and the participants with low serum 25(OH)D levels were thereafter r and omized to receive capsules of 20,000 IU vitamin D3 or identical-looking placebo twice weekly for 6 months . A final hyperglycemic clamp was then performed . RESULTS The 52 participants with high serum 25(OH)D levels ( 85.6 ± 13.5 nmol/L [ mean ± SD ] ) had significantly higher insulin sensitivity index ( ISI ) and lower HbA1c and triglycerides ( TGs ) than the 108 participants with low serum 25(OH)D ( 40.3 ± 12.8 nmol/L ) , but the differences in ISI and TGs were not significant after adjustments . After supplementation , serum 25(OH)D was 142.7 ± 25.7 and 42.9 ± 17.3 nmol/L in 49 of 51 completing participants r and omized to vitamin D and 45 of 53 r and omized to placebo , respectively . At the end of the study , there were no statistically significant differences in the outcome variables between the two groups . CONCLUSIONS Vitamin D supplementation to apparently healthy subjects with insufficient serum 25(OH)D levels does not improve insulin sensitivity or secretion or serum lipid profile OBJECTIVE To examine cross-sectional relationships between plasma vitamin D and cardiometabolic risk factors in young adults . DESIGN Data were collected from interviews , physical examinations and biomarker measurements . Total plasma 25-hydroxyvitamin D ( 25(OH)D ) was measured using LC-t and em MS . Associations between 25(OH)D and cardiometabolic risk factors were modelled using weighted linear regression with robust estimates of st and ard errors . SETTING Individuals born in Jerusalem during 1974 - 1976 . SUBJECTS Participants of the Jerusalem Perinatal Study ( n 1204 ) interviewed and examined at age 32 years . Participants were over sample d for low and high birth weight and for maternal pre-pregnancy obesity .  RESULTS Mean total 25(OH)D concentration among participants was 21·7 ( sd 8·9 ) ng/ml . Among males , 25(OH)D was associated with homeostatic model assessment of insulin resistance ( natural log-transformed , β=-0·011 , P=0·004 ) after adjustment for BMI . However , these associations were not present among females ( P for sex interaction=0·005 ) . CONCLUSIONS We found evidence for inverse associations of 25(OH)D with markers of insulin resistance among males , but not females , in a healthy , young adult Caucasian population . Prospect i ve studies and studies conducted on other population s investigating sex-specific effects of vitamin D on cardiometabolic risk factors are warranted It is unclear whether vitamin D lowers risk of type 2 diabetes ( T2D ) . In an observational study , we assessed the prospect i ve association between plasma  25-hydroxyvitamin D ( 25(OH)D )  and incident T2D  , and evaluated whether it holds up for genetically determined elevated 25(OH)D. We used a case-cohort study nested within the German arm of the European Prospect i ve Investigation into Cancer . From a total cohort of 53,088 participants with a mean follow-up of 6.6 years , we identified a r and om subcohort of 2,121 participants ( 57 % women ) and 1,572 incident cases of T2D .  25(OH)D was measured in baseline plasma sample s retrieved from frozen storage . Mean plasma 25(OH)D in the subcohort was 47.1 ( 5th–95th percentile 19.6–80.7 ) nmol/L. After controlling for age , sex , center , season of blood draw , education , and lifestyle , the hazard of T2D decreased across increasing plasma concentrations of 25(OH)D ( P linear trend < 0.0001 ) . The association became non-linear after adjustment for BMI and waist circumference ( P non-linearity < 0.0001 ) , with the inverse association being restricted to participants with 25(OH)D concentrations below ~45 nmol/L ( hazard ratio per 5 nmol/L higher 25(OH)D 0.91 , 95 % CI 0.84–0.98 ) . A score predicting genetically determined plasma 25(OH)D by weighting four independent single-nucleotide polymorphisms by their effect on 25(OH)D , explained 3.7 % of the variance in 25(OH)D. The hazard ratio ( 95 % CI ) per 5 nmol/L higher genetically predicted 25(OH)D was 0.98 ( 0.89–1.08 ) in the entire study sample and 1.06 ( 0.93–1.21 ) in the sub- sample with 25(OH)D < 45 nmol/L. This latter finding casts doubt on a strong causal association of 25(OH)D with T2D , but further research in large-scale consortia is needed Abstract Objective Patients with chronic kidney disease have a very high prevalence of deficiency of 25-hydroxyvitamin D [ 25(OH)D ] . We evaluate the association between 25(OH)D and diabetic nephropathy ( DN ) in a Chinese sample with type 2 diabetes mellitus . Method The subjects were patients with diabetes mellitus who were hospitalized at our hospital during the period from June 2012 to July 2014 .  Serum levels of 25(OH)D were tested at admission . DN was defined as a urinary albumin-to-creatinine ratio ≥30 mg/g in a r and om spot urine sample . Multivariate analyses were performed using logistic regression models . Results We found that serum 25(OH)D levels were significantly lower in diabetes with DN as compared to without DN [ 8.5 ( IQR 6.8–11.3 ) vs. 13.9 ( IQR 11.2–18.2 ) ng/ml , P < 0.0001 ] . Based on the ROC curve , the optimal cutoff value of serum 25(OH)D levels as an indicator for diagnosis of DN was projected to be 10.5 ng/ml , which yielded a sensitivity of 82.6 % and a specificity of 72.7 % , with the area under the curve at 0.807 [ 95 % confidence interval ( CI ) 0.764–0.849 ] . Multivariate logistic regression analysis adjusted for common risk factors showed that with serum 25(OH)D level ≤10.5 ng/ml was an independent indicator of DN [ odds ratio ( OR ) = 6.559 ; 95 % CI 2.864–11.368 ] . Conclusions Our findings suggested that diabetes with DN had lower serum 25(OH)D levels and that determination of 25(OH)D statuses might be used to identify patients at increased risk of developing nephropathy complications AIMS In recent years , there has been an effort to underst and possible roles of 25(OH)D , including its role in the immune system particularly on T cell medicated immunity , pancreatic insulin secretion and insulin action . 25(OH)D stimulates the cell differentiation and reduces cell proliferation , which is essential for cell growth and wound healing . However , data on the association between low level of plasma 25(OH)D and diabetic foot syndrome are scarce . MATERIAL S AND METHODS  Circulating plasma levels of 25(OH)D were  measured in diabetic patients with ulcer ( n=162 ) and without ulcer ( n=162 ) in a prospect i ve cohort hospital based study . RESULTS Of these patients , 85.1 % had type 2 diabetes . Subjects with diabetic foot ulcer showed lower median plasma level of 25(OH)D [ 6.3(4.2 - 11.1 ) vs 28.0(21.4 - 37.0 ) ] ng/ml after adjusting the age and BMI . Regardless of the low levels of 25(OH)D in cases and controls , it was associated with neuropathy , sex ( female ) , duration of ulcer healing , and smoking status and independent of confounding factors , including BMI ( kg/m² ) , A1c ( % ) , hypertension , nephropathy , foot ulcer , retinopathy , CAD , PAD , HDL-C ( mg/dl ) and LDL-C ( mg/dl ) . The factors which predict the risk of developing ulcer independent of 25(OH)D status were A1c ( > 6.9 % ) [ OR 4.37 ; RR 1.77 ] , HDL-C ( < 40mg/dl ) [ OR 1.16 ; RR 1.07 ] , LDL-C ( > 100mg/dl ) [ OR 1.07 ; RR 1.03 ] , triglycerides ( > 200mg/dl ) [ OR 1.40 ; RR 1.19 ] , neuropathy [ OR 6.88 ; RR 3.12 ] , retinopathy [ OR 3.34 ; RR 1.91 ] , hypertension [ OR 1.64 ; RR 1.28 ] , nephropathy [ OR 3.12 ; RR 1.87 ] and smoking [ OR 4.53 ; RR 2.99 ] using odds and risk ratios . CONCLUSION It is not clear whether the suppression of delayed wound healing seen during 25(OH)D deficiency is due to the secondary effect or is a direct action of vitamin D on certain components of the immune system . Long-term r and omized trials are needed to see the impact of vitamin D supplementation on the outcome of diabetic foot patients OBJECTIVES To examine whether ( 1 ) serum 25-hydroxyvitamin D level ( 25[OH]D ) is a risk factor for hyperglycemia , as assessed by glycated hemoglobin ( HbA1c ) , in African American men ( AAM ) and ( 2 ) 25(OH)D is a predictor of HbA1c in AAM and Caucasian American men ( CAM ) . METHODS We prospect ively assessed 25(OH)D and HbA1c in 1,074 men , out patients with and without diabetes , at an urban Veteran Administration Medical Center ( 66.8 % AAM , 26.4 % CAM , 6 % Hispanic , 0.4 % Asian , and 0.4 % Native American men ) . Multivariate regression analyzed the determinants of HbA1c after accounting for potential confounders . RESULTS We found high prevalence of low ( < 30 ng/mL ) 25(OH)D ( 81 % ) and elevated ( ≥5.7 % ) HbA1c ( 53.5 % ) . The 25(OH)D was inversely associated with HbA1c in all men ( r = -0.12 , P<.001 ) , in AAM ( r = -0.11 , P = .003 ) , and in CAM ( r = -0.15 , P = .01 ) . In the entire group the independent determinants of HbA1c included body mass index ( BMI ) , age , 25(OH)D levels , systolic blood pressure ( BP ) , triglycerides , high-density lipoprotein ( HDL ) , and current alcohol use ( P<.0001 , .013 , .009 , .01 , .008 , .034 , and .048 , respectively ) while glomerular filtration rate ( GFR ) and marital status showed borderline significance ( P = .08 and .09 , respectively ) . In AAM these determinants included BMI , 25(OH)D levels , systolic BP , and current alcohol use ( P<.0001 , .01 , .02 , and .03 , respectively ) , while age had borderline significance ( P = .06 ) . In CAM , these included BMI , age , and triglycerides ( P = .01 , .03 , and .004 , respectively ) but not 25(OH)D levels ( P = .50 ) . CONCLUSION Circulating low 25(OH)D is a risk factor for hyperglycemia , as assessed by HbA1c , in AAM . The 25(OH)D level is an independent determinant of HbA1c in AAM , but not in CAM , including men with and without diabetes OBJECTIVES To test the hypothesis that changes in DNA methylation are involved in vitamin D deficiency-related immune cell regulation using an unbiased genome-wide approach combined with a genomic and epigenomic integrative approach . STUDY DESIGN We performed a genome-wide methylation scan using the Illumina HumanMethylation 27 BeadChip on leukocyte DNA of 11 cases of vitamin D deficiency ( serum 25-hydroxyvitamin D [ 25(OH)D ] ≤ 25 nmol/L ) and 11 age-matched controls ( [ 25(OH)D ] > 75 nmol/L ) ; the subjects were African American normal-weight ( body mass index < 85th percentile ) males aged 14 - 19 years . The Limma package was used to analyze each CpG site for differential methylation between cases and controls . To correct for multiple testing , the set of raw P values were converted to false discovery rates ( FDRs ) . We also compared our findings with the recent data from Genome-Wide Association Studies of circulating 25(OH)D levels and then performed a permutation test to examine whether the " double hit " genes were r and omly enriched . RESULTS A total of 79 CpG sites achieved raw P < .001 . Of the 79 CpG sites , 2 CpG sites survived multiple testing : cg16317961 ( raw P = 3.5 × 10(-6 ) , FDR = 0.078 , in MAPRE2 ) and cg04623955 ( raw P = 5.9 × 10(-6 ) , FDR = 0.078 , in DIO3 ) . Furthermore , 3 out of the 4 genes previously identified in the 2 Genome-Wide Association Studies were also significant at the methylation level ( DHCR7 : cg07487535 , P = .015 and cg10763288 , P = .017 ; CYP2R1 : cg25454890 , P = .040 ; CYP24A1 : cg18956481 , P = .022 ) , reflecting significant enrichment ( P = .0098 ) . CONCLUSION Severe vitamin D deficiency is associated with methylation changes in leukocyte DNA . The genomic and epigenomic approach reinforce the crucial roles played by the DHCR7 , CYP2R1 , and CYP24A1 genes in vitamin D metabolism 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 Purpose This paper visualizes the available data on vitamin D status on a global map , examines the existing heterogeneities in vitamin D status and identifies research gaps . Methods A graphical illustration of global vitamin D status was developed based on a systematic review of the worldwide literature published between 1990 and 2011 . Studies were eligible if they included sample s of r and omly selected males and females from the general population and assessed  circulating 25-hydroxyvitamin D [ 25(OH)D ] levels .  Two different age categories were selected : children and adolescents ( 1–18 years ) and adults ( > 18 years ) . Studies were chosen to represent a country based on a hierarchical set of criteria . Results In total , 200 studies from 46 countries met the inclusion criteria , most coming from Europe . Forty-two of these studies ( 21 % ) were classified as representative . In children , gaps in data were identified in large parts of Africa , Central and South America , Europe , and most of the Asia/Pacific region . In adults , there was lack of information in Central America , much of South America and Africa . Large regions were identified for which the mean 25(OH)D levels were below 50 nmol/L. Conclusions This study provides an overview of 25(OH)D levels around the globe . It reveals large gaps in information in children and adolescents and smaller but important gaps in adults . In view of the importance of vitamin D to musculoskeletal growth , development , and preservation , and of its potential importance in other tissues , we strongly encourage new research to clearly define 25(OH)D status around the world
target: This meta- analysis concludes that hypovitaminosis D is associated with increased risk of hyperglycemia both in diabetic and non-diabetic subjects .
background: 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 .