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Integrative network toxicology and molecular docking preliminarily explore the potential role of polystyrene microplastics in childhood obesity
Summary
This study found that tiny plastic particles called polystyrene microplastics (found in food packaging and disposable cups) may contribute to childhood obesity by disrupting how the body processes fats and controls metabolism. The researchers discovered that these plastic particles can bind to and interfere with key genes responsible for managing cholesterol and insulin in the body. While more research is needed, these findings suggest parents should try to limit their children's exposure to disposable plastic food containers as a precaution against obesity risk.
Childhood obesity is a severe global epidemic, and emerging evidence suggests environmental pollutants like polystyrene microplastics (PS-MPs) may disrupt metabolic homoeostasis though mechanistic insights remain limited. This study integrated cross-species transcriptomics (from zebrafish and human adipose datasets), network toxicology, machine learning, and molecular docking to explore this link. We identified 40 overlapping genes between childhood obesity related DEGs and PS-MPs related genes, enriched in lipid metabolic pathways such as cholesterol homoeostasis and insulin signalling. Topological and machine-learning analyses highlighted hub genes, which showed strong diagnostic accuracy. Molecular docking further revealed stable binding (energy < -5.0 kcal/mol) between PS-MPs and key targets (APOB、BUB1、CDC20 and PPARGC1A). Our integrative analysis suggests that PS-MPs may act as an environmental trigger that could disrupt conserved lipid and metabolic homoeostasis by targeting key hub genes (APOB、BUB1、CDC20 and PPARGC1A). These findings provide a novel molecular hypothesis linking PS-MPs exposure to childhood obesity and support precautionary measures.
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