Insulin Resistance and Beta-Cell Function in the Context of Dyslipidemia in a Non-obese Indian Population With Type 2 Diabetes.
Abstract
Introduction Insulin resistance (IR) and impaired beta-cell function (BCF) are central to type 2 diabetes (T2D) pathogenesis and influence lipid metabolism, causing dyslipidemia. While most dyslipidemia studies focus on obese individuals, data on non-obese populations are limited. This study explored the association between IR, BCF, and lipid profiles in non-obese Indian T2D patients. Methods A cross-sectional analysis was conducted on T2D patients (n=667) with a body mass index <25 kg/m², not on insulin or lipid-lowering medications, who participated in a one-year lifestyle intervention program at the Freedom from Diabetes Clinic, India. Clinical, anthropometric, and biochemical data were extracted from existing records. IR and BCF were assessed using homeostatic model assessment of IR (HOMA2-IR) and BCF (HOMA2-%B). Results The median age, HbA1c, and diabetes duration were 50 years, 7.6%, and nine years, respectively. Overall, 73.3% (n=489) were male, 4.2% (n=28) had IR (HOMA2-IR≥2.0), and 69.9% (n=466) had reduced BCF (HOMA2-%B<50). HOMA2-IR showed a positive correlation with triglycerides and non-high-density lipoprotein cholesterol (non-HDL-C) (P<0.001) and a negative correlation with HDL-C (P<0.001). HOMA2-%B was negatively associated with total cholesterol, low-density lipoprotein cholesterol (LDL-C), non-HDL-C, and HDL-C (P<0.05). Receiver operating characteristic (ROC) analysis demonstrated that triglycerides (area under the curve (AUC)=0.648, P=0.008), non-HDL-C (AUC=0.626, P=0.023), and HDL-C in men (AUC=0.706, P=0.003) had fair discriminatory ability for IR. HOMA2-%B failed to discriminate lipid abnormalities. Conclusion In non-obese Indian T2D patients, both IR and beta-cell dysfunction are associated with dyslipidemia. However, only IR demonstrated a fair discriminatory ability for identifying abnormal lipid profiles, whereas BCF did not. These findings underscore the need for further studies to understand the metabolic drivers of lipid abnormalities in this population.
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