Clinical, Biochemical, and Inflammatory Correlates of Insulin Resistance in Patients Attending a Tertiary Care Teaching Centre: A Case-Control Study
Background: Insulin resistance is the earliest detectable lesion in the pathogenesis of type 2 diabetes mellitus (T2DM) and is closely linked to central adiposity, atherogenic dyslipidaemia, and chronic low-grade inflammation. South Asian populations, including Indians, develop insulin resistance at a younger age and lower body mass index than Western populations, making population-specific characterization important. Objective: To compare anthropometric, glycemic, lipid, and inflammatory/adipokine profiles between insulin-resistant subjects and matched insulin-sensitive controls attending a tertiary care teaching centre, and to identify clinical and biochemical correlates of insulin resistance severity. Methods: In this hospital-based case-control study, 60 insulin-resistant subjects (HOMA-IR ≥2.5) were compared with 60 age- and sex-matched controls. Anthropometric measures, fasting and post-glucose-load glycemic indices, a full lipid profile, and serum inflammatory markers (TNF-α, IL-6, hs-CRP) and adipokines (leptin, adiponectin, resistin) were assessed by validated laboratory methods. Results: Insulin-resistant subjects had significantly higher BMI, waist circumference, waist-hip ratio, and blood pressure than controls (p<0.001 for all). HOMA-IR was approximately 3.5-fold higher and QUICKI significantly lower in cases. An atherogenic dyslipidaemia pattern (elevated triglycerides, total cholesterol, LDL-C, VLDL-C; reduced HDL-C) was evident. TNF-α, IL-6, hs-CRP, leptin, and resistin were significantly elevated, while adiponectin was significantly reduced, in insulin-resistant subjects (p<0.001 for all). BMI correlated positively with TNF-α (r=+0.58) and negatively with adiponectin (r=−0.55). Conclusion: Insulin resistance in this tertiary care cohort is characterized by a coherent clinical phenotype of central adiposity, atherogenic dyslipidaemia, and chronic low-grade inflammation with adipokine dysregulation, consistent with obesity-driven inflammatory pathways described in the international literature and providing the clinical and biochemical substrate for the molecular signal-transduction abnormalities examined in a companion analysis.