Jul 2026· Journal of environmental biology· Vol 47, pp. 949-956· 0 citations
TL;DR
A comprehensive genetic and molecular landscape underlying childhood obesity is delineated, reflecting its multifactorial pathogenesis, with implications for improving future prevention and management strategies for childhood obesity.
Abstract
Aim: This study aimed to explore the genetic basis of childhood obesity through systematic identification and examination of genes, pathways, and regulatory elements contributing to disease development using integrated bioinformatic approaches.
Methodology: Thirty genes strongly associated with childhood obesity were subjected to detailed computational analysis using DisGeNET, Gene Ontology (GO), and WikiPathways. Gene–gene interaction patterns, biological processes, molecular functions, and cellular components were examined. Regulatory layers involving transcription factor and microRNA interactions were additionally analysed to characterise genetic and post-transcriptional control mechanisms.
Results: Significantly enriched pathways included adipogenesis, orexin receptor signalling, hunger and satiety regulation, and broader metabolic control mechanisms. Key genes including LEP, IL6, POMC and ADIPOQ recurred across multiple analyses, indicating central roles within obesity-associated molecular networks. Cross-database integration revealed complex genetic interactions and molecular cross-talk influencing obesity-related phenotypes.
Interpretation: This study delineates a comprehensive genetic and molecular landscape underlying childhood obesity, reflecting its multifactorial pathogenesis. The identification of key regulatory genes, transcription factors, and microRNA interactions provides valuable insight into potential molecular targets, with implications for improving future prevention and management strategies for childhood obesity.
Key words: Bioinformatics, Childhood obesity, Gene pathways, Molecular networks, Therapeutic targets
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