Bisphenol A exposure and its impact on childhood obesity: a molecular and genetic perspective.

Abstract

Childhood obesity is a growing public health concern, with emerging evidence suggesting that environmental factors like bisphenol A (BPA) exposure may contribute to its development. This study aims to elucidate the genetic and molecular mechanisms linking BPA exposure to childhood obesity. We analyzed the publicly available dataset GSE9624 to identify differentially expressed genes (DEGs) associated with childhood obesity. We cross-referenced these DEGs with BPA-related toxicity targets obtained from the Comparative Toxicogenomics Database (CTD) and SwissTargetPrediction database. Network construction, molecular docking, enrichment analysis, Gene Set Variation Analysis (GSVA), and correlation analysis were performed to explore interactions between BPA exposure and childhood obesity. We identified 967 DEGs associated with childhood obesity, with 81 overlapping BPA-related toxicity targets. A heatmap revealed distinct expression patterns of these genes between obese and normal-weight children. Network analysis highlighted JUN, TOP2A, APOE, and LEP as hub genes. Molecular docking indicated strong binding affinities between BPA and these core targets. Enrichment analysis revealed disruptions in lipid metabolism, cell cycle, and oxidative stress pathways. GSVA demonstrated significant differences in oxidative stress, inflammatory response, and lipid metabolism between obese and normal-weight children. Correlation analysis further conformed BPA's impact on metabolic-immune pathways through core genes modulation. Our findings suggest that BPA exposure may drive childhood obesity by disrupting metabolic, inflammatory, and oxidative stress pathways. The identified core genes and pathways provide a molecular basis for further research and potential therapeutic targets in BPA-related metabolic disorders.