INFLAMMATORY AND ENDOCRINE MECHANISMS LINKING PEDIATRIC OBESITY TO INSULIN RESISTANCE
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Pediatric obesity has emerged as a major global health concern, closely associated with the early development of metabolic disorders. Among these, insulin resistance represents a central pathophysiological mechanism linking excess adiposity to type 2 diabetes and cardiometabolic complications. Increasing evidence suggests that chronic low-grade inflammation and endocrine dysregulation play pivotal roles in this process. Visceral adiposity promotes the release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which interfere with insulin signaling pathways. Simultaneously, adipokine imbalance—characterized by elevated leptin levels and reduced adiponectin concentrations—further impairs insulin sensitivity. Alterations in hypothalamic regulation, mitochondrial dysfunction, oxidative stress, and gut microbiota changes have also been implicated in the development of insulin resistance in obese children.
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