Model of BPA action on pancreatic β-cells.
In the presence of stimulatory glucose concentrations, low concentrations of BPA rapidly decrease KATP channel activity through ERβ, enhancing glucose-induced [Ca2+]i signals and insulin release. ERα is involved in the regulation of pancreatic insulin biosynthesis in response to BPA. In addition to ERβ, GPR30/GPER1 or another yet unidentified non-classical membrane estrogen receptor may participate in the insulinotropic effect of BPA on pancreatic β-cells. At the moment, this model applies to rodent beta cells. In humans, the receptors involved in the BPA regulation of KATP channel activity and insulin release are still undetermined.