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Bisphenol A: What lies beneath its induced diabetes and the epigenetic modulation?

Soheila Rahmani, Nazila Pour Khalili, Fazlullah Khan, Shokoufeh Hassani, Elmira Ghafour-Boroujerdi, Mohammad Abdollahi
Life sciences 2018 v.214 pp. 136-144
DNA methylation, adipocytes, animals, bisphenol A, demethylation, endocrine-disrupting chemicals, epigenetics, estrogenic properties, fatty liver, genes, glucose, histones, homeostasis, insulin, islets of Langerhans, lipids, liver, microRNA, noninsulin-dependent diabetes mellitus, obesity, pollution, skeletal muscle, toxicity
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.