ArticleScientific reports2026
PCB-126 exposure promotes brown adipose tissue dysfunction and metabolic inflexibility in mice.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Polychlorinated biphenyls (PCBs) remain a global health concern due to their persistence and toxicity. PCB-126, a potent aryl hydrocarbon receptor (AhR) agonist, is linked to metabolic disruption, yet its impact on brown adipose tissue (BAT) is not fully understood. Male C57BL/6 mice were exposed to PCB-126 (5 µmol/kg) for 10 weeks, followed by morphological, biochemical, and molecular interscapular brown adipose tissue (iBAT) analyses. Despite comparable energy intake and delta body weight, PCB-126 markedly increased relative visceral fat and reduced relative iBAT mass. Oral glucose tolerance testing revealed impaired glucose handling, with higher glycemia across the curve and a ~ 30% increase in AUC, indicating systemic metabolic dysfunction. Histology showed extensive lipid droplet remodeling—reduced lipid area fraction but increased droplet number—consistent with a blunted thermogenic phenotype. At the molecular level, PCB-126 downregulated thermogenic markers (Ucp1, Prdm16, Pgc-1α, Adrb3) and Vegfa, reflecting impaired vascularization. Genes involved in lipid droplet regulation (Cidea), adipogenic control (Pparγ), and energy-sensing (Ampk2) were also suppressed, reinforcing thermogenic loss and reduced metabolic flexibility. These changes coincided with heightened inflammation (Tnf-α, Il-6), oxidative stress (↑MDA, ↑NOx), and compromised antioxidant defenses (↓SOD, ↓catalase, ↑GPx). Overall, PCB-126 disrupts BAT structure and transcriptional programming, impairs glucose tolerance, and promotes visceral fat accumulation through combined thermogenic, inflammatory, and redox dysregulation.
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