The Role of Leptin and Insulin Resistance in the Onset of Precocious Puberty among Obese Pediatric Patients

Abstract

Objective: To determine the relationship between insulin resistance, leptin, and CPP in obese children and to clarify their diagnostic role. Study Design: Cross-sectional studyPlace and Duration of Study: This study was conducted at the Pediatric Endocrinology Outpatient Clinic Iraq from 15th May 2025 to 14th October 2025. Methods: 90 children ages 5–10 years were enrolled. They were divided into three groups of healthy (Group A), obese without puberty (Group B), and obese with central precocious puberty (Group C). Each group consisted of 30 children. Pubertal signs, fasting insulin, homeostatic model assessment for insulin resistance, leptin, and hormonal profile were assessed. Central precocious puberty predictors were determined using logistic regression and receiver operating characteristic curves. Results: The degree of leptin actually escalated: 3.22, 1.8, with the groups (A), 12.4, 4.7 (B), 18.9, 6.3 (C). The same was true of homeostatic model assessment for insulin resistance: (1.5 + 0 7), (4.4 + 1.8), and (5.9±2.3) respectively. luteinizing hormone was very high in group C. Homeostatic model assessment for insulin resistance (r=0.78) and body mass index Z-score (r=0.82) were significantly related to leptin. Leptin 14.2 ng/mL or greater predicted central precocious puberty was definite sensitivity (90 %) and specificity (87%). Conclusion: The evidence confirms the bi-functional location of leptin in the metabolic/reproductive endocrine system, which solidly attaches this molecule to insulin resistance and the emergence of central precocious puberty. Leptin and homeostatic model assessment for insulin resistance as independent predictors were validated using multivariate analysis.