Leptin-to-Adiponectin Ratio is Related to Low Grade Inflammation and Insulin Resistance Independent of Obesity in Non-Diabetic Taiwanese: A Cross-Sectional Cohort Study

Background: Leptin and adiponectin are secreted from adipose tissue and exert opposing effects on C-reactive protein (CRP) levels and insulin resistance. As hypertrophic adipocytes secrete more leptin and less adiponectin, the leptin-to adiponectin ratio (LAR) has been proposed as a useful measure of insulin resistance and vascular risk. We investigated whether LAR may serve as a better predictor than either leptin or adiponectin alone for low-grade inflammation and insulin resistance independent of obesity in a non-diabetic Taiwanese population. Methods: This study included 568 non-diabetic Taiwanese individuals (297 men, 271 women). CRP, leptin and adiponectin were measured using enzyme-linked immunosorbent assay. The degree of insulin resistance was determined using the homeostasis model assessment of insulin resistance (HOMA-IR). Results: In the receiver operator characteristic analysis, the area under the curve of LAR in predicting individuals with elevated CRP and insulin resistance was significantly greater than that for either leptin (p = 0.0035 vs. elevated CRP, p < 0.0001 vs. insulin resistance) or adiponectin alone (p = 0.0131 vs. elevated CRP, p = 0.0006 vs. insulin resistance), suggesting that LAR might be a better predictor of individuals with low grade inflammation and insulin resistance. In the multivariable analysis adjusted for age, gender, smoking status, and components of metabolic syndrome, LAR was still strongly associated with levels of CRP (p < 0.001, all participant; p = 0.002, nonobese individuals; p < 0.001, obese individuals) and HOMA-IR index (p < 0.001, all participants, obese and nonobese individuals). Conclusions: The LAR is related to low grade inflammation and insulin resistance independent of obesity in non-diabetic Taiwanese, and the strength of associations between LAR with CRP and HOMMR are greater than the association with leptin or adiponectin alone.