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Significance Exposure of pregnant female mice to bisphenol A (BPA) results in obesity in the F2 progeny, which can be transmitted in the absence of additional exposure up to the… Click to show full abstract
Significance Exposure of pregnant female mice to bisphenol A (BPA) results in obesity in the F2 progeny, which can be transmitted in the absence of additional exposure up to the F6 generation. Obesity results from increased food consumption and its transmission correlates with the presence of a chromatin accessible site in a cis-regulatory element (CRE) present in an intron of the Fto gene, which becomes demethylated after BPA exposure. This CRE interacts with the Irx3 and Irx5 genes, which are involved in the differentiation of appetite-controlling neurons in the hypothalamus. Mice carrying a deletion of the CTCF site fail to become obese after exposure to BPA, suggesting that epigenetic changes in a CTCF site are responsible for transgenerational inheritance of obesity.
Journal Title: Proceedings of the National Academy of Sciences of the United States of America
Year Published: 2022
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