Background: Type 2 diabetes mellitus (T2DM) is characterized by chronic hyperglycaemia, insulin resistance, and progressive β-cell dysfunction. The pancreas functions as an integrated endocrine–exocrine organ, and increasing evidence suggests that metabolic derangements in T2DM may also affect exocrine pancreatic function. Obesity further amplifies insulin resistance, promotes diabetic dyslipidaemia, and contributes to pancreatic fat deposition, potentially influencing pancreatic enzyme secretion. Serum amylase has emerged as a simple biochemical surrogate of exocrine pancreatic activity in metabolic states. Objectives: To assess the correlation between fasting plasma glucose and serum amylase among obese patients with type 2 diabetes mellitus; To assess the correlation between lipid profile parameters and serum amylase among obese patients with type 2 diabetes mellitus. Methods: This descriptive cross-sectional study was conducted in a tertiary care teaching hospital in Salem during March – June 2024. 50 obese patients (BMI >30 kg/m²) with T2DM attending the outpatient department were included by purposive sampling. Fasting plasma glucose, lipid profile (total cholesterol, triglycerides, HDL, LDL, VLDL, TC/HDL ratio), and serum amylase were estimated using standard biochemical methods. Pearson’s correlation was applied to assess associations. Results: The mean age of participants was 54.2 ± 6.2 years, with male predominance (68%). Mean fasting plasma glucose was 146.82 ± 23.02 mg/dl. The lipid profile demonstrated an atherogenic pattern, and mean serum amylase levels were relatively low (28.30 ± 7.64 IU/L). Serum amylase showed a strong inverse correlation with fasting plasma glucose (r = −0.831, p < 0.01), triglycerides, VLDL, total cholesterol, LDL, and TC/HDL ratio, and a strong positive correlation with HDL cholesterol (p < 0.01). Conclusion: Serum amylase is inversely associated with hyperglycaemia, atherogenic dyslipidaemia, and duration of diabetes in obese T2DM patients, supporting a close endocrine–exocrine–metabolic linkage.
Rajalakshmi et al. (Tue,) studied this question.