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.