Adipogenic effects of prenatal exposure to bisphenol S (BPS) in adult F1 male mice

Bisphenol S (BPS) has been increasingly used as a substitute for bisphenol A (BPA), a known endocrine disruptor. Early-life exposure to BPA affects fetal development and the risk of obesity in adolescence and adulthood. However, the effects of fetal exposure BPS in later life are unknown. This study aimed to investigate the effects of prenatal BPS exposure on adiposity in adult F1 mice. Pregnant C57BL/6 N mice were exposed to BPS (0, 0.05, 0.5, 5, and 50 mg/kg/d) via drinking water from gestation day 9 until delivery. Thereafter, two groups of offspring (6 weeks old) were either administered a standard diet (STD) or a high-fat diet (HFD) for 4 weeks until euthanasia. The body weight and gonadal white adipose tissue (gWAT) mass were determined, and the energy expenditure for the adiposity phenotype was computed especially for male mice, followed by histological analysis of the gWAT. Thereafter, the expression levels of adipogenic marker genes (Pparg, Cebpa, Fabp4, Lpl, and Adipoq) were analyzed in the gWAT via reverse-transcription PCR analysis. BPS-exposed male mice displayed apparent gWAT hypertrophy, consistent with the significant increase in adipocyte size in the gWAT and upregulation of Pparg and its direct target genes among HFD mice in comparison with the control mice. These results suggest that prenatal BPS exposure potentially increases the susceptibility to HFD-induced adipogenesis in male adult mice. [Display omitted] •BPS has been used increasingly with insufficient evidence of toxicity.•Prenatal BPS exposure caused gonadal adipocyte hypertrophy in high-fat-fed mice.•Adipogenic genes were upregulated in the enlarged gonadal adipose tissues.•In utero BPS exposure affects the adipogenic susceptibility in male mice.