What question did this study set out to answer?

This research aims to investigate the effects of PCB-126 on brown adipose tissue and metabolic inflexibility in mice.

February 11, 2026Scientific Reports0 citationsOpen Access

PCB-126 exposure promotes brown adipose tissue dysfunction and metabolic inflexibility in mice

TPThamara Cherem PeixotoUniversidade do Estado do Rio de Janeiro CMCarolline Santos MirandaUniversidade do Estado do Rio de Janeiro ATAlessandra Marques Rangel TeixeiraUniversidade do Estado do Rio de Janeiro

Key Points

This research aims to investigate the effects of PCB-126 on brown adipose tissue and metabolic inflexibility in mice.
Male C57BL/6 mice exposed to PCB-126 for 10 weeks at 5 µmol/kg
Morphological and biochemical analysis of interscapular brown adipose tissue
Glucose tolerance testing to evaluate metabolic function
Histological assessment of lipid droplet changes
Molecular analysis of thermogenic and inflammatory markers
PCB-126 exposure increased relative visceral fat and reduced relative brown adipose tissue mass
Impaired glucose tolerance indicated by increased glycemia and AUC
Histological alterations showed increased lipid droplet number but reduced lipid area
Downregulation of thermogenic markers such as Ucp1 and Prdm16
Increased inflammation and oxidative stress components were noted.

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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