European Journal of Cardiovascular Medicine

Type 2 diabetes mellitus (T2DM) is one of the most important non-communicable diseases of the twenty-first century. The International Diabetes Federation estimated that 463 million adults were living with diabetes worldwide in 2019, and that India accounted for about 77 million of them, second only to China [1]. The ICMR-INDIAB study, covering 15 states of India, showed that diabetes and prediabetes affect a large and growing share of the population, with considerable variation between states [2]. Earlier Indian work had already described the early onset, strong familial clustering and high central adiposity that characterise diabetes in South Asians [3], and the Global Burden of Disease analysis confirmed a steep rise in the burden of diabetes in every Indian state between 1990 and 2016 [4]. Because chronic hyperglycemia drives microvascular and macrovascular complications, achieving and maintaining good glycemic control remains the central goal of care.

Vitamin D is a fat-soluble secosteroid hormone best known for its role in calcium and bone homeostasis. Its deficiency is now recognised as a global public health problem, affecting people of all ages in both temperate and tropical regions [5,6]. The Endocrine Society defines deficiency as a serum 25-hydroxyvitamin D [25(OH)D] level below 20 ng/mL and insufficiency as 21-29 ng/mL [7], although the Institute of Medicine regards levels of 20 ng/mL as adequate for most of the population [8]. India presents a paradox: despite plentiful sunshine, surveys from the north and the south report a high prevalence of low 25(OH)D in apparently healthy adults, children and pregnant women [9-11]. Skin pigmentation, atmospheric pollution, indoor lifestyles, clothing practices, vegetarian diets low in vitamin D and calcium, and high dietary phytate have all been proposed as contributors [12-14].

A biological rationale connects vitamin D with glucose metabolism. Pancreatic beta cells express the vitamin D receptor and the enzyme 1-alpha-hydroxylase, and early experimental work showed that vitamin D deficiency impairs insulin secretion [15]. Mice lacking a functional vitamin D receptor show reduced insulin secretory capacity [16], and a vitamin D response element has been identified in the promoter of the human insulin receptor gene, suggesting that vitamin D may also influence insulin sensitivity [17]. Vitamin D may further act through calcium-dependent signalling, modulation of inflammatory cytokines and regulation of the renin-angiotensin system [18-20].

Observational data support these mechanisms. In the Third National Health and Nutrition Examination Survey, serum 25(OH)D was inversely related to the prevalence of diabetes in some ethnic groups [21], and low 25(OH)D has been linked to insulin resistance and beta-cell dysfunction [22]. Prospective cohorts suggest that baseline 25(OH)D predicts later glycemic status and insulin resistance [23,24]. Systematic reviews support an association between vitamin D status and the risk of T2DM, although the evidence from randomised trials has been less consistent [25-28]. Indian studies have reported a high prevalence of vitamin D deficiency in people with diabetes and in those at high metabolic risk [29-31], but data relating 25(OH)D levels to the degree of glycemic control in routine hospital practice remain limited, and published Indian series differ in design and cut-offs.

Identifying a modifiable factor associated with poor glycemic control would have practical value, because vitamin D testing and supplementation are inexpensive and widely available. The present study was therefore designed to determine the vitamin D status of patients with T2DM attending a tertiary care hospital and to examine its relationship with glycemic control.

1.1 Aim and objectives

To estimate the prevalence of vitamin D deficiency and insufficiency in patients with type 2 diabetes mellitus. To compare serum 25(OH)D levels across categories of glycemic control defined by HbA1c. To assess the correlation between serum 25(OH)D and fasting plasma glucose, postprandial plasma glucose and HbA1c. To identify factors associated with vitamin D deficiency in this population.

2.1 Study design, setting and duration

This was a hospital-based, observational, cross-sectional study conducted in the Department of General Medicine of a tertiary care teaching hospital in India over a period of 12 months (January 2022 to December 2022). Patients were recruited from both outpatient and inpatient services.

2.2 Sample size

The sample size was calculated using the formula n = Z²pq/d², where Z = 1.96 for 95% confidence, p is the expected prevalence of vitamin D deficiency, q = 1 - p, and d is the absolute precision. Taking an anticipated prevalence of 50% (the most conservative assumption) and an absolute precision of 7%, the minimum sample size was 196. A total of 200 patients were enrolled by consecutive sampling.

2.3 Inclusion and exclusion criteria

Inclusion criteria: adults aged 30-75 years with T2DM diagnosed according to the American Diabetes Association criteria [32] (fasting plasma glucose ≥126 mg/dL, 2-hour plasma glucose ≥200 mg/dL, HbA1c ≥6.5%, or established treatment for diabetes) who gave written informed consent.

Exclusion criteria: (i) type 1 diabetes, gestational diabetes or secondary diabetes; (ii) use of vitamin D, calcium or multivitamin supplements, or anti-obesity drugs, in the preceding six months; (iii) chronic kidney disease (eGFR <60 mL/min/1.73 m²), chronic liver disease or malabsorption syndromes; (iv) known parathyroid, thyroid or bone disease; (v) use of drugs affecting vitamin D metabolism (anticonvulsants, rifampicin, glucocorticoids); (vi) pregnancy or lactation; and (vii) acute illness or diabetic ketoacidosis at presentation.

2.4 Data collection

After consent, a pre-tested structured proforma was used to record age, sex, residence, occupation, duration of diabetes, treatment, history of hypertension, dietary habit (vegetarian or mixed) and average daily sun exposure (<30 minutes or ≥30 minutes between 10 am and 3 pm). Weight and height were measured with standard instruments and body mass index (BMI) was calculated as weight (kg) divided by height squared (m²). Because of the higher metabolic risk at lower BMI in Asian Indians, overweight was defined as BMI ≥25 kg/m² [33]. Blood pressure was recorded after five minutes of rest.

2.5 Laboratory investigations

After an overnight fast of 8-10 hours, 5 mL of venous blood was collected. Fasting plasma glucose and 2-hour postprandial plasma glucose were measured by the glucose oxidase-peroxidase method. HbA1c was estimated by high-performance liquid chromatography (HPLC) certified by the National Glycohemoglobin Standardization Program. Serum 25(OH)D and intact parathyroid hormone (PTH) were measured by chemiluminescent immunoassay. Serum calcium, phosphorus, creatinine and the lipid profile were measured on a fully automated analyser. Samples were processed within two hours of collection.

2.6 Operational definitions

Vitamin D status was classified using serum 25(OH)D as deficient (<20 ng/mL), insufficient (20-29.9 ng/mL) or sufficient (≥30 ng/mL) [7]. Glycemic control was classified by HbA1c as good (<7.0%), fair (7.0-8.9%) or poor (≥9.0%), with the 7% threshold being the general target recommended for most non-pregnant adults [34]. For logistic regression, HbA1c ≥7% was considered inadequate control.

2.7 Ethical considerations

The study was approved by the Institutional Ethics Committee (approval number. All participants received information about the study, and written informed consent was obtained. Confidentiality was maintained, and patients found to be vitamin D deficient were treated according to standard guidelines.

2.8 Statistical analysis

Data were entered in Microsoft Excel and analysed with SPSS version 25.0 (IBM Corp., Armonk, NY, USA). Continuous variables are expressed as mean ± standard deviation and categorical variables as number (percentage). Differences between three groups were assessed by one-way ANOVA with post hoc Bonferroni correction, and between two groups by the independent-samples t test. The chi-square test was used for categorical variables. Pearson's correlation coefficient assessed the relationship between serum 25(OH)D and continuous variables. Multivariable linear regression was used to identify independent predictors of HbA1c, and binary logistic regression to estimate the adjusted odds ratio (OR) of inadequate glycemic control with vitamin D deficiency, after adjusting for age, sex, BMI, duration of diabetes and sun exposure. A two-sided p value <0.05 was considered statistically significant

A total of 200 patients with T2DM fulfilled the criteria and were included in the final analysis. No patient was lost to follow-up of the laboratory protocol.

3.1 Baseline characteristics

The mean age of the study population was 52.4 ± 10.8 years, and the largest proportion of patients (38.0%) belonged to the 50-59 year age group. There were 108 men (54.0%) and 92 women (46.0%). The mean duration of diabetes was 7.8 ± 5.1 years and the mean BMI was 27.1 ± 4.2 kg/m², with 64.0% of patients overweight by Asian criteria. Hypertension coexisted in 49.0%, 59.0% had sun exposure of less than 30 minutes per day, and 56.0% were vegetarian (Table 1).

Table 1: Baseline demographic and clinical characteristics of the study population (N = 200)

3.2 Biochemical profile

The mean fasting and postprandial plasma glucose values were 166.7 ± 51.8 mg/dL and 238.7 ± 69.6 mg/dL, and the mean HbA1c was 8.1 ± 1.6%. The mean serum 25(OH)D was 19.9 ± 9.3 ng/mL. Mean serum calcium and phosphorus were within normal limits, whereas mean intact PTH was at the upper end of the reference range (Table 2).

Table 2: Biochemical parameters of the study population (N = 200)

3.3 Vitamin D status

Of the 200 patients, 96 (48.0%) were vitamin D deficient, 71 (35.5%) were insufficient and only 33 (16.5%) had sufficient levels. Thus, 83.5% of patients had suboptimal vitamin D status (Table 3, Figure 1).

Table 3: Distribution of patients according to vitamin D status

.4 Vitamin D status and glycemic control

According to HbA1c, 62 patients (31.0%) had good control (<7%), 74 (37.0%) fair control (7.0-8.9%) and 64 (32.0%) poor control (≥9%). The mean serum 25(OH)D declined progressively across these groups, from 26.8 ± 8.9 ng/mL in the good control group to 19.7 ± 7.6 ng/mL in the fair control group and 13.4 ± 6.2 ng/mL in the poor control group (ANOVA F = 52.3, p<0.001; Table 4, Figure 2). Post hoc analysis showed that each pair of groups differed significantly (p<0.001 for good versus fair and fair versus poor).

Table 4: Mean serum 25(OH)D levels according to glycemic control (HbA1c)

One-way ANOVA: F = 52.3, p<0.001. Values are mean ± SD.

The distribution of vitamin D categories within each glycemic group is shown in Table 5. Vitamin D deficiency was present in 68.8% of patients with poor control and 51.4% with fair control, but in only 22.6% of those with good control, whereas 32.3% of patients with good control had sufficient vitamin D compared with 12.5% and 6.8% in the poor and fair groups, respectively (chi-square = 40.1, p<0.001).

Table 5: Vitamin D status across glycemic control groups, n (%)

Chi-square test: χ² = 40.1, df = 4, p<0.001.

Conversely, glycemic indices were significantly higher in patients with vitamin D deficiency. Mean HbA1c was 8.7 ± 1.5% in the deficient group, 7.8 ± 1.4% in the insufficient group and 6.8 ± 1.1% in the sufficient group (p<0.001). Fasting and postprandial plasma glucose followed the same gradient (Table 6).

Table 6: Glycemic parameters according to vitamin D status

One-way ANOVA. Values are mean ± SD.

3.5 Correlation analysis

Serum 25(OH)D showed a significant negative correlation with HbA1c (r = -0.58, p<0.001), fasting plasma glucose (r = -0.49, p<0.001), postprandial plasma glucose (r = -0.46, p<0.001), PTH (r = -0.42, p<0.001), duration of diabetes (r = -0.31, p<0.001) and BMI (r = -0.27, p<0.001). A weak positive correlation was seen with serum calcium (r = 0.18, p = 0.011), while no significant correlation was found with age (Table 7, Figure 3).

Table 7: Pearson correlation of serum 25(OH)D with clinical and biochemical variables

NS = not significant.

.6 Factors associated with vitamin D deficiency

Vitamin D deficiency was significantly more frequent in women (63.0% versus 35.2% in men), in patients with sun exposure of less than 30 minutes per day (59.3% versus 31.7%), in those with BMI ≥25 kg/m² (55.5% versus 34.7%) and in vegetarians (55.4% versus 38.6%). No significant association was found with hypertension or with residence (Table 8).

Table 8: Factors associated with vitamin D deficiency (<20 ng/mL)

Chi-square test.

3.7 Regression analysis

In the multivariable linear regression model with HbA1c as the dependent variable, serum 25(OH)D (β = -0.041 per ng/mL; 95% CI -0.054 to -0.028; p<0.001), duration of diabetes and BMI were independent predictors, while age and sex were not. The model explained 46% of the variance in HbA1c (adjusted R² = 0.46; Table 9). Each 10 ng/mL fall in 25(OH)D was therefore associated with an approximately 0.4 percentage-point rise in HbA1c after adjustment.

Table 9: Multivariable linear regression for predictors of HbA1c

Adjusted R² = 0.46.

On binary logistic regression, 82 of 96 vitamin D deficient patients (85.4%) had HbA1c ≥7%, compared with 56 of 104 (53.8%) of non-deficient patients. The crude odds of inadequate glycemic control were five-fold higher in the deficient group (OR 5.02; 95% CI 2.53-9.95; p<0.001). After adjustment for age, sex, BMI, duration of diabetes and sun exposure, vitamin D deficiency remained independently associated with inadequate control (adjusted OR 3.74; 95% CI 1.78-7.85; p<0.001).

This cross-sectional study of 200 patients with T2DM found that hypovitaminosis D is the rule rather than the exception in this population and that lower serum 25(OH)D is strongly and independently associated with poorer glycemic control. Nearly half of the patients (48.0%) were frankly deficient and a further 35.5% were insufficient, so that fewer than one in five had sufficient levels.

The high prevalence of deficiency observed here is consistent with the Indian studies. Early surveys from Delhi documented low 25(OH)D concentrations in a majority of healthy adults [9], and later studies from rural north India and from the south showed that low vitamin D status persists across latitudes and socioeconomic strata. Reviews of the Indian data estimate that deficiency affects a very large proportion of the population, depending on the cut-off used . Among people with diabetes, Indian investigators have likewise reported a high burden of low vitamin D, including in young adults and in those with metabolic syndrome [29-31]. Hypovitaminosis D is also a worldwide problem, so the finding is not unique to India. The slightly higher prevalence in our sample compared with some general-population figures may reflect the indoor lifestyle, higher BMI and age of hospital attendees, and the use of the 20 ng/mL cut-off for deficiency.

The central finding of this study is the stepwise decline in mean 25(OH)D from 26.8 ng/mL in patients with good control to 13.4 ng/mL in those with poor control, with a correlation of r = -0.58 with HbA1c. Similar inverse relationships between 25(OH)D and HbA1c in T2DM have been described by other investigators [35]. Population-based data also show that people with higher 25(OH)D have lower odds of metabolic syndrome and diabetes [36], and prospective analyses suggest that low baseline 25(OH)D predicts higher subsequent glycemia and insulin resistance. In a study of Asian Indians, vitamin D deficiency was associated with the components of metabolic syndrome, supporting the relevance of this relationship to the Indian phenotype. Our multivariable model indicates that the association is not explained merely by duration of diabetes or adiposity, since 25(OH)D remained significant after adjustment, and patients with vitamin D deficiency had almost four times the adjusted odds of inadequate control.

Several mechanisms could explain the association. Vitamin D influences insulin secretion through the beta-cell vitamin D receptor and through calcium flux, as pancreatic insulin release is calcium dependent; deficiency impairs secretion in experimental models. In humans, hypovitaminosis D has been related to both insulin resistance and beta-cell dysfunction. Transcriptional effects on the insulin receptor gene and effects on inflammatory cytokines may further modulate insulin sensitivity. Secondary hyperparathyroidism may also contribute: the significant inverse correlation of 25(OH)D with PTH in our patients (r = -0.42) and the higher PTH in deficient patients is in line with this pathway, although a causal role of PTH in insulin resistance remains unproven.

The relationship is also likely to be bidirectional. Adiposity sequesters vitamin D in adipose tissue and lowers its bioavailability [37], and Asian Indians accumulate visceral fat at relatively low BMI. We found an inverse correlation between BMI and 25(OH)D, and vitamin D deficiency was more common in overweight patients. Poorly controlled diabetes may itself reduce outdoor activity, increase urinary losses of vitamin D-binding protein, or be associated with reduced physical activity and sun exposure, so reverse causation cannot be excluded in a cross-sectional design.

Deficiency was more common in women, in those with limited sun exposure, in overweight patients and in vegetarians. Indian studies have repeatedly shown that sun avoidance, covered clothing, urban indoor occupations, skin pigmentation and diets low in vitamin D and calcium but high in phytate are important determinants. The greater deficiency among women observed here is in keeping with reports from Indian cohorts and may reflect clothing habits, indoor domestic work and repeated pregnancies and lactation. Food fortification and community sunlight-exposure advice have been proposed as population-level measures.

Whether correcting vitamin D deficiency improves glycemic control is a separate question that an observational study cannot answer. Meta-analyses of supplementation trials in non-diabetic and diabetic populations have reported modest or inconsistent effects on glycemia and insulin resistance and some small trials in T2DM have reported improved insulin sensitivity after vitamin D therapy [38]. Large randomised trials in people with prediabetes, notably the D2d trial, did not show a statistically significant reduction in progression to diabetes with vitamin D3 compared with placebo whereas a pooled analysis suggested a modest benefit in participants with prediabetes. These data suggest that supplementation is unlikely to replace established glucose-lowering therapy, but they do not diminish the value of detecting and treating deficiency in its own right, particularly in a population with high skeletal and cardiometabolic risk. Our results justify evaluating vitamin D status in patients whose glycemic control is poor despite apparently adequate therapy.

Strengths and limitations

Strengths of this study include the use of standardised laboratory methods (HPLC-based HbA1c, immunoassay for 25(OH)D and PTH), the exclusion of patients on supplements or interfering drugs, and adjustment for key confounders. The limitations are the single-centre, cross-sectional design, which precludes inference of causality; the absence of insulin resistance indices (HOMA-IR) and C-peptide; the lack of data on dietary vitamin D and calcium intake, physical activity, skin type and seasonal variation; and a convenience sample from a tertiary centre, which may over-represent patients with complicated disease. Diabetes treatment regimens, which influence HbA1c, were not included in the model. Multi-centre prospective studies and randomised trials in Indian patients with T2DM are warranted.

Vitamin D deficiency and insufficiency are highly prevalent among patients with type 2 diabetes mellitus, affecting more than four out of five patients in this study. Lower serum 25(OH)D was significantly associated with higher fasting and postprandial glucose and HbA1c, and vitamin D deficiency was independently associated with inadequate glycemic control. Screening for vitamin D status should be considered as part of the comprehensive evaluation of patients with T2DM, particularly those with poor control, obesity, limited sun exposure or a vegetarian diet. Well-designed interventional studies are needed to determine whether correcting vitamin D deficiency improves glycemic outcomes in this population.

1. Saeedi P, Petersohn I, Salpea P, Malanda B, Karuranga S, Unwin N, et al. Global and regional diabetes prevalence estimates for 2019 and projections for 2030 and 2045: results from the International Diabetes Federation Diabetes Atlas, 9th edition. Diabetes Res Clin Pract. 2019;157:107843.
2. Anjana RM, Deepa M, Pradeepa R, Mahanta J, Narain K, Das HK, et al. Prevalence of diabetes and prediabetes in 15 states of India: results from the ICMR-INDIAB population-based cross-sectional study. Lancet Diabetes Endocrinol. 2017;5(8):585-96.
3. Mohan V, Sandeep S, Deepa R, Shah B, Varghese C. Epidemiology of type 2 diabetes: Indian scenario. Indian J Med Res. 2007;125(3):217-30.
4. Tandon N, Anjana RM, Mohan V, Kaur T, Afshin A, Ong K, et al. The increasing burden of diabetes and variations among the states of India: the Global Burden of Disease Study 1990-2016. Lancet Glob Health. 2018;6(12):e1352-62.
5. Holick MF. Vitamin D deficiency. N Engl J Med. 2007;357(3):266-81.
6. Mithal A, Wahl DA, Bonjour JP, Burckhardt P, Dawson-Hughes B, Eisman JA, et al. Global vitamin D status and determinants of hypovitaminosis D. Osteoporos Int. 2009;20(11):1807-20.
7. Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, et al. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2011;96(7):1911-30.
8. Ross AC, Manson JE, Abrams SA, Aloia JF, Brannon PM, Clinton SK, et al. The 2011 report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: what clinicians need to know. J Clin Endocrinol Metab. 2011;96(1):53-8.
9. Goswami R, Gupta N, Goswami D, Marwaha RK, Tandon N, Kochupillai N. Prevalence and significance of low 25-hydroxyvitamin D concentrations in healthy subjects in Delhi. Am J Clin Nutr. 2000;72(2):472-5.
10. Sahu M, Bhatia V, Aggarwal A, Rawat V, Saxena P, Pandey A, et al. Vitamin D deficiency in rural girls and pregnant women despite abundant sunshine in northern India. Clin Endocrinol (Oxf). 2009;70(5):680-4.
11. Harinarayan CV, Ramalakshmi T, Prasad UV, Sudhakar D, Srinivasarao PV, Sarma KV, et al. High prevalence of low dietary calcium, high phytate consumption, and vitamin D deficiency in healthy south Indians. Am J Clin Nutr. 2007;85(4):1062-7.
12. Harinarayan CV, Joshi SR. Vitamin D status in India - its implications and remedial measures. J Assoc Physicians India. 2009;57:40-8.
13. Ritu G, Gupta A. Vitamin D deficiency in India: prevalence, causalities and interventions. Nutrients. 2014;6(2):729-75.
14. Aparna P, Muthathal S, Nongkynrih B, Gupta SK. Vitamin D deficiency in India. J Family Med Prim Care. 2018;7(2):324-30.
15. Norman AW, Frankel JB, Heldt AM, Grodsky GM. Vitamin D deficiency inhibits pancreatic secretion of insulin. Science. 1980;209(4458):823-5.
16. Zeitz U, Weber K, Soegiarto DW, Wolf E, Balling R, Erben RG. Impaired insulin secretory capacity in mice lacking a functional vitamin D receptor. FASEB J. 2003;17(3):509-11.
17. Maestro B, Davila N, Carranza MC, Calle C. Identification of a vitamin D response element in the human insulin receptor gene promoter. J Steroid Biochem Mol Biol. 2003;84(2-3):223-30.
18. Palomer X, Gonzalez-Clemente JM, Blanco-Vaca F, Mauricio D. Role of vitamin D in the pathogenesis of type 2 diabetes mellitus. Diabetes Obes Metab. 2008;10(3):185-97.
19. Mathieu C, Gysemans C, Giulietti A, Bouillon R. Vitamin D and diabetes. Diabetologia. 2005;48(7):1247-57.
20. Sung CC, Liao MT, Lu KC, Wu CC. Role of vitamin D in insulin resistance. J Biomed Biotechnol. 2012;2012:634195.
21. Scragg R, Sowers M, Bell C. Serum 25-hydroxyvitamin D, diabetes, and ethnicity in the Third National Health and Nutrition Examination Survey. Diabetes Care. 2004;27(12):2813-8.
22. Chiu KC, Chu A, Go VL, Saad MF. Hypovitaminosis D is associated with insulin resistance and beta cell dysfunction. Am J Clin Nutr. 2004;79(5):820-5.
23. Forouhi NG, Luan J, Cooper A, Boucher BJ, Wareham NJ. Baseline serum 25-hydroxy vitamin D is predictive of future glycemic status and insulin resistance: the Medical Research Council Ely Prospective Study 1990-2000. Diabetes. 2008;57(10):2619-25.
24. Knekt P, Laaksonen M, Mattila C, Harkanen T, Marniemi J, Heliovaara M, et al. Serum vitamin D and subsequent occurrence of type 2 diabetes. Epidemiology. 2008;19(5):666-71.
25. Pittas AG, Lau J, Hu FB, Dawson-Hughes B. The role of vitamin D and calcium in type 2 diabetes. A systematic review and meta-analysis. J Clin Endocrinol Metab. 2007;92(6):2017-29.
26. Mitri J, Muraru MD, Pittas AG. Vitamin D and type 2 diabetes: a systematic review. Eur J Clin Nutr. 2011;65(9):1005-15.
27. Pittas AG, Dawson-Hughes B, Sheehan P, Ware JH, Knowler WC, Aroda VR, et al. Vitamin D supplementation and prevention of type 2 diabetes. N Engl J Med. 2019;381(6):520-30.
28. Zhang Y, Tan H, Tang J, Li J, Chong W, Hai Y, et al. Effects of vitamin D supplementation on prevention of type 2 diabetes in patients with prediabetes: a systematic review and meta-analysis. Diabetes Care. 2020;43(7):1650-8.
29. Sheth JJ, Shah A, Sheth FJ, Trivedi G, Shah S, Shah S, et al. Does vitamin D play a significant role in type 2 diabetes? BMC Endocr Disord. 2015;15:5.
30. Daga RA, Laway BA, Shah ZA, Mir SA, Kotwal SK, Zargar AH. High prevalence of vitamin D deficiency among newly diagnosed youth-onset diabetes mellitus in north India. Arq Bras Endocrinol Metabol. 2012;56(7):423-8.
31. Majumdar V, Nagaraja D, Christopher R. Vitamin D status and metabolic syndrome in Asian Indians. Int J Obes (Lond). 2011;35(8):1131-4.
32. American Diabetes Association. 2. Classification and diagnosis of diabetes: Standards of Medical Care in Diabetes-2021. Diabetes Care. 2021;44(Suppl 1):S15-33.
33. Misra A, Khurana L. Obesity and the metabolic syndrome in developing countries. J Clin Endocrinol Metab. 2008;93(11 Suppl 1):S9-30.
34. American Diabetes Association. 6. Glycemic targets: Standards of Medical Care in Diabetes-2021. Diabetes Care. 2021;44(Suppl 1):S73-84.
35. Kostoglou-Athanassiou I, Athanassiou P, Gkountouvas A, Kaldrymides P. Vitamin D and glycemic control in diabetes mellitus type 2. Ther Adv Endocrinol Metab. 2013;4(4):122-8.
36. Ford ES, Ajani UA, McGuire LC, Liu S. Concentrations of serum vitamin D and the metabolic syndrome among U.S. adults. Diabetes Care. 2005;28(5):1228-30.
37. Wortsman J, Matsuoka LY, Chen TC, Lu Z, Holick MF. Decreased bioavailability of vitamin D in obesity. Am J Clin Nutr. 2000;72(3):690-3.
38. Talaei A, Mohamadi M, Adgi Z. The effect of vitamin D on insulin resistance in patients with type 2 diabetes. Diabetol Metab Syndr. 2013;5(1):8.