Role of Adiponectin in Modulating Insulin Resistance in Visceral Obesity-Associated Type 2 Diabetes Mellitus

Abstract

Background: Visceral obesity is a key determinant of insulin resistance and pathogenesis of type 2 diabetes mellitus (T2DM). Adiponectin is an adipokine predominantly secreted by visceral adipose tissue, characterized by potent anti-inflammatory and insulin-sensitizing properties. The reduction of adiponectin in obesity may contribute to metabolic dysfunction. A comprehensive understanding of its regulatory functions offers valuable insights into the underlying pathophysiology. The aim of the study was to evaluate the role of serum adiponectin in modulating insulin resistance among patients with visceral obesity-associated T2DM and to examine its association with anthropometric and metabolic parameters.

Methods: This cross-sectional study included 140 adults (aged 30 - 65) with T2DM and confirmed visceral obesity (waist circumference (WC) ≥ 90 cm in men, ≥ 80 cm in women). Serum adiponectin, fasting glucose and insulin levels were measured using enzyme-linked immunosorbent assay and chemiluminescent immunoassay. Insulin resistance was assessed via the homeostatic model assessment for insulin resistance (HOMA-IR) index. Spearman correlations and multivariate regression analyses were performed.

Results: Serum adiponectin levels were significantly lower in individuals with elevated HOMA-IR (P < 0.01). Adiponectin showed a strong inverse correlation with HOMA-IR (ρ = -0.45, P < 0.001), body mass index (BMI, ρ = -0.17, P = 0.041), WC (ρ = -0.23, P = 0.006) and fasting glucose (ρ = -0.79, P < 0.001). Multivariate regression confirmed adiponectin as an independent predictor of insulin resistance after adjusting for age, gender, WC and BMI.

Conclusion: Adiponectin is a key modulator of insulin resistance in visceral obesity-associated T2DM. Its inverse relationship with HOMA-IR, central adiposity and dyslipidemia underscores its role as a sensitive biomarker and potential therapeutic target for improving metabolic health.