Model of BPA action on pancreatic β-cells.

In the presence of stimulatory glucose concentrations, low concentrations of BPA rapidly decrease K_ATP 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 K_ATP channel activity and insulin release are still undetermined.