Vol. 1, Issue 1, Part G (2014)

Methods: A cross-sectional analytical study was conducted on 45 adults (40–60 years) with T2DM (<5 years of duration) and overweight or grade I obesity, without hyperuricemia. Clinical parameters including BMI, blood pressure, and lipid profile were assessed, and insulin secretion phases were analyzed using the hyperglycemic clamp technique. Serum uric acid, fasting insulin, glucose, HbA1c, and lipid levels were measured using standardized enzymatic and immunoassay techniques. Pearson’s correlation analysis was performed to determine associations between uric acid and insulin secretion phases, adjusting for BMI and other confounders.

Results: A significant positive correlation was observed between serum uric acid levels and total insulin secretion (r = 0.310, P = 0.052). After adjusting for BMI, this correlation increased in strength (r = 0.439, P = 0.024), suggesting that uric acid influences insulin secretion independently of adiposity. The first-phase insulin secretion showed the strongest correlation with uric acid (r = 0.306, P = 0.055), indicating that uric acid primarily affects early-phase insulin release rather than sustained secretion. These findings align with previous studies suggesting uric acid modulates beta-cell function and compensatory insulin responses.

Conclusion: This study provides new insights into the metabolic role of uric acid in insulin secretion, demonstrating that even in normouricemic individuals, uric acid levels correlate with early-phase insulin secretion. These findings suggest that uric acid may act as a compensatory factor in beta-cell function and could serve as a biomarker for insulin dynamics in T2DM. Future research should explore molecular mechanisms and potential therapeutic implications of targeting uric acid metabolism in diabetes management.