Nowadays, endocrine disrupting chemical pollution has become one of the major concerns due to the potential role of these chemicals in provoking endocrine disorders especially type 2 diabetes. As a widespread endocrine disrupting chemical, Bisphenol A, with modest estrogenic activity can exert its detrimental effects in the different organs involved in type 2 diabetes such as pancreas, liver, adipocyte and skeletal muscles. Obesity, hepatic steatosis, impaired insulin signaling and pancreatic islet function could be the main results of Bisphenol A exposure. Epigenetic dysregulations can be suggested as an important underlying mechanism for Bisphenol A toxicity in the endocrine system. The most studied genes in this respect, which are responsible for glucose homeostasis include Pdx1, Gck, Igf2, Srebf1 and Srebf2. Aberrant DNA methylation, histone demethylation and deacetylation and impaired miRNAs result in epigenetically dysfunctional genes that finally distract the normal glucose regulation. The present study aimed to summarize the general effects of prenatal and postnatal Bisphenol A exposure on glucose metabolism focusing on animal studies and review the recent investigations on Bisphenol A -induced epigenetic perturbations that affect the normal glucose and lipid homeostasis and lead to type 2 diabetes.
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This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canada's national genomics strategy with $900 million in funding from the federal government.