Abstract

Rapid estrogen actions are triggered after estrogens are bound to a variety of proteins in organelles other than the nucleus. Those include classic estrogen receptors ERα and ERβ, novel membrane proteins that behave as estrogen receptors such as GPR30, ion channels, and other ligand receptors. In pancreatic α and β-cells, estrogens binding to a non-classical membrane estrogen receptors at physiological concentrations regulate ion channels and [Ca2+]i signals, provoking important physiological responses. In β-cells, 17β- estradiol regulates KATP channel activity and glucose-induced [Ca2+]i oscillations, eliciting changes in insulin release and the activation of Ca2+-dependent transcription factors. In α-cells, 17β-estradiol abolishes low glucose-induced [Ca2+]i oscillations.