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The obesogenic effects of Bisphenol A and its analogues are differentially regulated via PPARγ transactivation in

Jennifer Crosthwait¹, Syed Syeddan¹, Ella Atlas²

¹Environmental Health Science and Research Bureau (EHSRB), Health Canada, 251 Sir Frederick Banting Driveway, Ottawa, Ontario K1A 0K9, Canada.

Toxicology in Vitro : an International Journal Published in Association with BIBRA

|January 22, 2025

Abstract:

Exposure to environmental pollutants with obesogenic activity is being recognised as one of the contributing factors to the obesity epidemic. Bisphenol A (BPA) has been shown to stimulate adipogenesis in both human and mouse preadipocytes, to increase body weight and affect lipid metabolism in animal and epidemiological studies. Regulatory action and public concern has prompted industry to replace BPA with other structurally similar analogues that may have similar effects. In this study we investigated the effects of fifteen BPA analogues on adipogenesis in the mouse 3 T3-L1 pre-adipocyte cell model in order to determine their adipogenic activity relative to BPA. 3 T3-L1 cells were treated with increasing concentrations of BPA and replacements and mRNA expression of the mature adipocyte markers fatty acid binding protein 4 (Fabp4), perilipin (Plin) lipoprotein lipase (Lpl)and peroxisome proliferator-activated receptor (Ppar)γ and lipid accumulation were assessed. In addition, a luciferase reporter assay for PPARγ transactivation was employed to investigate mechanism of action. Our results show that BPC, BPS-MAE, BPS-MPE and TGSA, were the most adipogenic bisphenols, as shown by a robust increase in lipid accumulation and mRNA expression of adipogenic markers. BPS-MPE, BPC, BTUM, TGSA and D8 increased PPARγ transcriptional activity. Despite its ability to activate PPARγ in the transcriptional assay D8 did not affect adipogenesis in this cell model.

Keywords:

3T3-L1 Adipogenesis Bisphenol A Bisphenol A analogues Obesity

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