Ripoll Cristina, Ropero Ana B, Alonso-Magdalena Paloma, Quesada Ivan, Fuentes Esther, Nadal Angel
Instituto de Bioingeniería, Universidad Miguel Hernández de Elche y CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Instituto de Salud Carlos III, Elche 03202, Alicante, Spain.
Infect Disord Drug Targets. 2008 Mar;8(1):61-4. doi: 10.2174/187152608784139668.
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 alpha and beta-cells, estrogens binding to a non-classical membrane estrogen receptors at physiological concentrations regulate ion channels and Ca(2+) signals, provoking important physiological responses. In beta-cells, 17beta-estradiol regulates K(ATP) channel activity and glucose-induced Ca(2+) oscillations, eliciting changes in insulin release and the activation of Ca(2+)-dependent transcription factors. In alpha-cells, 17beta-estradiol abolishes low glucose-induced Ca(2+) oscillations.
