Rapid Regulation of Pancreatic alpha- and beta- Cell Signalling Systems by Estrogens

摘要

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 ERalpha and ERbeta novel membrane proteins that behave as estrogen receptors such as GPR30, ion channels, and other ligand receptors. In pancreatic a and p-cells, estrogens binding to a non-classical membrane estrogen receptors at physiological concentrations regulate ion channels and Ca~(2+)i signals, provoking important physiological responses. In p-cells, 17p-estradiol regulates K_(ATP) channel activity and glucose-induced Ca~(2+)j oscillations, eliciting changes in insulin release and the activation of Ca~(2+)-dependent transcription factors. In alpha-cells, 17p-estradiol abolishes low glucose-induced Ca~(2+)j oscillations.