METABOLIC AND ENDOCRINE CONSEQUENCES OF CHILDHOOD OBESITY: FROM INSULIN RESISTANCE TO NON-ALCOHOLIC FATTY LIVER DISEASE

Childhood obesity is associated with a complex constellation of metabolic and endocrine disturbances that, if unaddressed, predict adult chronic disease with high fidelity. Objective: This review examines the specific metabolic pathways through which excess adiposity in childhood leads to insulin resistance, type 2 diabetes mellitus (T2DM), dyslipidemia, non-alcoholic fatty liver disease (NAFLD), and reproductive endocrine disorders. Methods: Systematic narrative review of clinical studies, endocrinological investigations, and population cohort data from 2008 to 2024. Results: Adipose tissue expansion drives inflammatory cytokine production, free fatty acid spillover, and ectopic lipid deposition. These processes produce hepatic and peripheral insulin resistance, progressive β-cell dysfunction, non-alcoholic steatohepatitis, and in adolescent girls, polycystic ovarian syndrome. Conclusion: Early identification and intervention targeting metabolic comorbidities of childhood obesity are essential to preventing a generation-wide chronic disease epidemic.儿童肥胖与一系列复杂的代谢及内分泌紊乱密切相关，若未加以干预，可高度精准地预判成年慢性疾病的发生风险。研究目的：本综述旨在阐明儿童时期体脂过量引发胰岛素抵抗、2型糖尿病（type 2 diabetes mellitus, T2DM）、血脂异常、非酒精性脂肪性肝病（non-alcoholic fatty liver disease, NAFLD）及生殖内分泌紊乱的具体代谢通路。方法：本研究针对2008年至2024年间的临床研究、内分泌学调研及人群队列数据开展系统性叙述性综述。结果：脂肪组织扩张可促进促炎细胞因子生成、游离脂肪酸溢出及异位脂质沉积。上述过程可引发肝脏及外周组织胰岛素抵抗、进行性β细胞功能障碍、非酒精性脂肪性肝炎（non-alcoholic steatohepatitis），且在青春期女性中可诱发多囊卵巢综合征（polycystic ovarian syndrome）。结论：针对儿童肥胖相关代谢共病开展早期识别与干预，对于预防整代人群的慢性疾病流行至关重要。