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Research Article Volume 14 Issue 1
Multifactorial architecture of pediatric obesity: from genetic susceptibility to systemic metabolic dysfunction
Voroncova TO, Zubnina YO, Khlibovska OI, Dzhyvak VH
Received: February 17, 2026 | Published: March 2, 2026
Citation: Voroncova TO, Zubnina YO, Khlibovska OI, et al. Multifactorial architecture of pediatric obesity: from genetic susceptibility to systemic metabolic dysfunction. Endocrinol Metab Int J. 2026;14(1):10-14. DOI: 10.15406/emij.2026.14.00383
Abstract
Pediatric obesity has evolved into a formidable global pandemic, representing a complex, chronic metabolic disorder that fundamentally compromises the physiological and psychosocial development of the younger generation. This research provides an exhaustive, multifaceted analysis of the etiology of childhood adiposity, dissecting the synergistic interplay between polygenic susceptibility, epigenetic modifications, and the modern obesogenic environment. By characterizing adipose tissue as a high-functioning, albeit dysfunctional, endocrine organ, the study elucidates the molecular pathways leading to chronic low-grade systemic inflammation, profound insulin resistance, and early-onset metabolic syndrome. Special emphasis is placed on the cholecalciferol-insulin axis and the «metabolic memory» ingrained through intrauterine programming. The findings advocate for an urgent shift toward precision endocrinology and multidisciplinary intervention to mitigate the escalating burden on global healthcare systems.
Keywords: pediatric obesity, adipogenesis, neuroendocrine dysregulation, FTO/MC4R genes, insulin resistance, metabolic syndrome, cholecalciferol (Vitamin D3), epigenetic programming, DOHaD concept, public health strategy
©2026 Voroncova, et al. This is an open access article distributed under the terms of the, which permits unrestricted use, distribution, and build upon your work non-commercially.