Fetal origins of metabolic disease
Fetal exposure to the endocrine disrupting chemical bisphenol A (BPA) causes insulin resistance in the adult (Veiga-Lopez et al., Am J Physiol – Endocrinol Metab 2016), a pre-stage of type 2 diabetes, which affects ~350 million people. In women, gestational BPA exposure affects the newborn’s weight in a sex-specific manner (Veiga-Lopez et al., J Clin Endocrinol Metab 2015). Animal studies suggest that weight increases are due to increase body fat. How BPA induces insulin resistance and weight gain/obesity remains unknown. Our research using in vivo and cell-based assays aims to understand the mechanistic basis by which BPA programs insulin resistance and obesity during fetal life. Our work has demonstrated for the first time that gestational BPA can increase the ability of fetal primary preadipocytes to differentiate into mature adipocytes and points to the endoplasmic reticulum stress as a potential modulator in this effect. (Pu et al., Endocrinology 2017). Our recent work has also focused on another insulin target tissue, the skeletal muscle. We have demonstrated sex- and bisphenol-specific effects on myocytes upon prenatal exposures (Jing et al., Toxicological Sciences 2020).
Check out our review on the effects of endocrine disrupting chemicals on adipogenesis (Obesogenic endocrine disrupting chemicals: identifying knowledge gaps. Trends in Endocrinology & Metabolism 2018).
This work was funded by an NIEHS/NIH K22 TIEHR award.