According to the International Diabetes Federation, there were more than 72.9 million cases of diabetes in India by 2017.1

Since the 1980s, the global rate of diabetes has almost doubled, going from 4.75% to 8.55% in adults. This is because more people are at risk, like being overweight or obese. In the last ten years, diabetes has been growing much faster in low- and middle-income countries than in high-income countries.2

Diabetes mellitus is a long-term metabolic disorder that can be caused by not making enough insulin or by the insulin that the pancreas makes not working properly. A lack of this substance causes the blood to have more glucose, which can hurt many of the body's normal functions, especially the nerves and blood vessels.3

Diabetes mellitus (DM) and hyperglycemia share the same phenotype. A complicated mix of genetics and environmental factors causes a number of different types of DM. The factors that lead to high blood sugar levels in people with diabetes mellitus (DM) depend on what caused the DM. These factors include less insulin being made, less glucose being used, and more glucose being made. Type 2 Diabetes can manifest as primarily insulin resistance coupled with relative insulin deficiency or as a predominant insulin secretory defect accompanied by insulin resistance.4

Type 2 Diabetes Mellitus exhibits significant familial aggregation; however, it is only recently that specific genes have been consistently linked to an elevated risk of Type 2 diabetes in particular populations. Both types of diabetes are complicated illnesses caused by changes in more than one gene and a small number of environmental factors.5

About 1 billion people worldwide have a vitamin D deficiency. This could be because they don't get enough sunlight, wear clothes that cover their skin for a long time, use sunscreen, or eat foods that contain ergocalciferol. It could also be because they have malabsorption syndrome. In the last ten years, scientists have paid a lot more attention to the link between vitamin D and insulin insensitivity or abnormal glucose metabolism. Different observations or links were mentioned. Investigating the potential involvement of modified vitamin D status and its metabolites or altered insulin sensitivity in the pathogenesis of each disease.6

The precise mechanisms by which vitamin D exerts its multifaceted effects on various tissues remain incompletely elucidated; however, a distinctive aspect is the expression of vitamin D receptors (VDRs) in over 30 tissues, including pancreatic islet cells. Some evidence indicates that polymorphisms in the VDR gene may be linked to insulin resistance, insulin secretion, and fasting glucose levels, implying that vitamin D likely plays a role in glucose metabolism.7

 OBJECTIVES:

1. To evaluate the prevalence of vitamin D deficiency in Type 2 Diabetic Population.
2. To assess the correlation between Vitamin D levels and glycaemic control.

Study was carried out on Type 2 diabetes mellitus patients visited the General Medicine outpatient department and also type 2 diabetes mellitus patients admitted to the General Medicine wards at HIMS Hassan met inclusion and exclusion criteria. 150 patients

 Sampling method:  Convenient sampling.

Study duration: 1 Year (June 2024 – May 2025)

Methods of collection of data

After obtaining clearance and approval from Institutional Ethics Committee, a Cross-sectional Observational study was conducted from Department of General Medicine, Hassan Institute of Medical Sciences, Hassan, GRMC Mangalore and Subbaiah institute of medical sciences Shivamoga

Patients with type 2 diabetes mellitus visiting General medicine and type 2 diabetes mellitus patients admitted in the Medicine wards were selected according to the inclusion and exclusion criteria mentioned below:

 Inclusion Criteria

• Age more than 18yrs.
• Type 2 diabetes mellitus patients attending medicine opd and admitted in ward
• Type 2 Diabetes mellitus patients on treatment either with diet or diet and oral antidiabetic drugs or Insulin.

 Exclusion Criteria

• Patients with established chronic kidney disease
• Patients with established chronic liver disease
• Patients on glucocorticoid therapy for any cause
• Patients on anti-seizure medications
• Patients on vitamin D or calcium supplements
• Patients with type 1 diabetes
• Pregnant woman
• Patients with bone disease

 Methodology and follow-up

After getting approval from Institutional ethics committee, written informed consent was taken. Patients with Type 2 diabetes mellitus visiting the medicine OPD was selected according to inclusion and exclusion criteria. The aims and objectives of the intended study was properly explained to the subject. Detailed history taken regarding duration of diabetes mellitus, medications patient currently on, other comorbidities like hypertension, acute coronary syndrome. Initial consultation and examination involved the routine assessment of Serum 25(OH)D and glycaemic control (HbA1c) concentration and also followed by laboratory parameters was done including (complete blood count, blood sugar, lipid profile, renal function test, liver function test). Serum concentration of 25(OH) D was measured by enzyme linked immunosorbent assay (ELISA) method. HbA1c measured by spectrophotometer.  Patients were classified according to their HbA1c level into the followings: <5.7% (normal), 5.7%–6.4% (prediabetes), > =6.5% (diabetes) and≥7% (uncontrolled diabetes). Following cut-off values were used to classifying vitamin D status as follows: A normal level of vitamin D is defined as a 25(OH)D con-centration greater than 30 ng/mL, vitamin D insufficiency is defined as a 25(OH)D concentration of 20–30 ng/mL, and vitamin D deficiency is defined as a 25(OH)D level less than 20 ng/ mL.

Table 1: Glycemic Profile of the Study Population

A majority of participants exhibited poor glycemic control (72.0%), while only 28.0% had good control. This suggests suboptimal glycemic regulation in most subjects. Poor glycemic control may influence metabolic and urinary parameters in the study population.

HbA1c levels among the study participants ranged from 4.86% to 9.88%, with a mean value of 7.53 ± 1.00%, indicating overall suboptimal long-term glycemic control. Fasting blood sugar levels varied widely between 98.9 mg/dL and 251.5 mg/dL, with a mean of 170.22 ± 31.73 mg/dL, reflecting poor fasting glycemic regulation in many participants. Postprandial blood sugar values ranged from 90.0 mg/dL to 354.0 mg/dL, with a mean of 216.74 ± 49.99 mg/dL. The higher mean PPBS compared to FBS suggests greater postprandial hyperglycemia.

 Table 2: Distribution of Vitamin D Status Among Study Participants

Vitamin D deficiency was observed in 44.0% of participants, followed closely by insufficiency in 42.7%. Only 13.3% of subjects had normal Vitamin D levels. This highlights a high prevalence of suboptimal Vitamin D status in the study population. Serum 25-hydroxy vitamin D levels among the study participants ranged from 5.0 ng/mL to 43.8 ng/mL. The mean vitamin D level was 20.95 ± 8.32 ng/mL, indicating overall low to insufficient vitamin D status in the population. The wide range of values reflects considerable variability in vitamin D levels among individuals. These findings suggest a high prevalence of hypovitaminosis D in the study group.

 Table 3: Comparison of Glycemic and Vitamin D Parameters According to Vitamin D Status

HbA1c (%)

Mean HbA1c values were comparable across Vitamin D deficient (7.42 ± 1.00%), insufficient (7.65 ± 0.98%), and normal groups (7.47 ± 1.06%). The observed differences were not statistically significant (p = 0.408). Glycemic control as assessed by HbA1c did not differ based on Vitamin D status.

Fasting Blood Sugar (mg/dL)

The mean fasting blood sugar levels were similar in the deficient (167.32 ± 32.05 mg/dL), insufficient (174.75 ± 30.34 mg/dL), and normal groups (165.33 ± 34.73 mg/dL). The difference was not statistically significant (p = 0.314). This indicates comparable fasting glycemic levels across Vitamin D categories.

 Table 4: Medication Pattern According to Vitamin D Status

 Medication Pattern

Medication usage patterns were comparable across Vitamin D categories, with oral antidiabetic drugs being the most commonly used treatment in all groups. Insulin alone and combined OAD with insulin therapy were distributed similarly among deficient, insufficient, and normal groups. The association between medication pattern and Vitamin D status was not statistically significant (p = 0.518).

 Table 5: Serum Calcium Levels and Serum Calcium Status According to Vitamin D Status

Serum Calcium (mg/dL)

Mean serum calcium levels were similar among deficient (9.15 ± 0.51 mg/dL), insufficient (9.15 ± 0.52 mg/dL), and normal groups (9.20 ± 0.49 mg/dL). No statistically significant difference was observed (p = 0.907). Serum calcium levels did not vary with Vitamin D status.

 Serum Calcium Status

Most participants across all Vitamin D categories had normal serum calcium levels, accounting for 84.8% of deficient, 85.9% of insufficient, and 95.0% of normal groups. Low serum calcium was observed more frequently in deficient and insufficient groups compared to the normal group. However, the association between serum calcium status and Vitamin D levels was not statistically significant (p = 0.492).

The present research study was undertaken to evaluate the correlation between the serum 25-hydroxyvitamin D levels and the glycaemic control among patients with Type 2 Diabetes Mellitus attending the tertiary care hospital.8 Type 2 Diabetes Mellitus is a complex metabolic disorder which is characterized by insulin resistance and relative insulin deficiency, and its prevalence is increasing rapidly in developing countries, including India. In recent years, vitamin D deficiency has gained the attention as a potentially modifiable factor influencing the glucose metabolism, insulin secretion, and the insulin sensitivity.9

According to glycaemic assessment, only 28% (n = 42) of patients had good glycaemic control, while 72% (n = 108) had poor glycaemic control (HbA1c ≥ 7%). The average HbA1c level was 7.53 ± 1.00%, which indicates generally less than ideal long-term glycaemic control. These results are similar to those of Al Dossari et al., who found that a significant percentage of patients had mean HbA1c values above recommended targets and that 36.5% of their cohort had poor glycaemic control.10

The current study's mean post-prandial blood sugar (PPBS) was 216.74 ± 49.99 mg/dL, and the mean fasting blood sugar (FBS) level was 170.22 ± 31.73 mg/dL. Harrison's Textbook of Medicine4 states that the higher PPBS compared to FBS indicates predominant post-prandial hyperglycemia, a pattern commonly seen in Indian populations as a result of dietary habits and insulin resistance. According to Hyppönen et al., there is a strong correlation between negative metabolic profiles and elevated post-prandial glucose levels.11

In this study, the mean HbA1c levels were similar in the groups with low vitamin D (7.42 ± 1.00%), not enough vitamin D (7.65 ± 0.98%), and normal vitamin D (7.47 ± 1.06%). There was no statistically significant difference (p = 0.408). While the glycemic control was generally superior in the individuals with normal vitamin D levels, the correlation did not achieve the statistical significance.12

When glycemic control was broken down, 24.2% of patients with low vitamin D levels, 25.0% of patients with normal vitamin D levels, and 50.0% of patients with normal vitamin D levels had good control.13 On the other hand, people who didn't get enough vitamin D (75.8%) or who didn't get enough vitamin D (75.0%) had poor glycemic control. This trend suggests that sufficient vitamin D levels may offer protection; however, the correlation was not statistically significant (p = 0.062).

Al Dossari et al. found that patients with poor glycemic control (82%) had a much higher rate of vitamin D deficiency than those with good control (52%). They also found a statistically significant link between lower vitamin D levels and higher HbA1c values.1 In a similar vein, Salih et al. showed that patients with poor glycemic control had much lower serum 25(OH)D levels than those with good control (p < 0.001).2 The absence of statistical significance in this study may be due to variations in study design, population characteristics, and a comparatively shorter duration of diabetes.14-15

The average fasting blood sugar levels in this study were 167.32 ± 32.05 mg/dL for the vitamin D deficient group, 174.75 ± 30.34 mg/dL for the insufficient group, and 165.33 ± 34.73 mg/dL for the normal group. The differences were not statistically significant (p = 0.314), which means that the fasting blood sugar levels were similar across all vitamin D groups.

Need et al. found a strong negative link between fasting serum glucose and serum 25(OH)D levels, especially when vitamin D levels were less than 40 ng/mL.8Hyppönen et al. also showed that there is a negative relationship between vitamin D levels and markers of glucose homeostasis, such as fasting glucose, in a large population-based study.9 The lack of a significant link in this study could be due to the fact that antidiabetic drugs can make fasting glucose levels normal even when insulin resistance is present.16

Hypovitaminosis D is very common in people with Type 2 Diabetes Mellitus. The strong link between vitamin D levels and blood sugar levels after meals suggests that vitamin D may play a role in controlling blood sugar levels after meals. This shows how important it is to check vitamin D levels as part of regular diabetes care.

1. International Diabetes Federation - IDF Diabetes Atlas (Eighth edition) 2017 https://www.idf.org/
2. Global Report on Diabetes 2016; WHO Library Cataloguing-in-Publication Data (http://www.who.int/diabetes/en/)
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4. Alvin C Powers, Harrison’s textbook of Medicine 19th edition, Diabetes Mellitus Chapter 417 page no 2399.
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