Open Access
Article
Role of estrogen receptors alpha, beta and GPER1/GPR30 in pancreatic beta-cells
Angel Nadal1,Paloma Alonso-Magdalena1,Sergi Soriano1,Cristina Ripoll1,Esther Fuentes1,Ivan Quesada1,Ana Belen Ropero1
1
CIBER de Diabetes y Enfermedades Metabolicas Asociadas and Instituto de Bioingenieria, Universidad Miguel Hernandez de Elche, Elche, Spain. nadal@umh.es
DOI: 10.2741/3686 Volume 16 Issue 1, pp.251-260
Published: 01 January 2011
(This article belongs to the Special Issue Estrogen receptors in lipid raft signalling)
Abstract

Estrogen receptors (ER) are emerging as important molecules involved in the adaptation of beta-cells to insulin resistance. The onset of type 2 diabetes is marked by insulin secretory dysfunction and decreased beta-cell mass. During pregnancy, puberty and obesity there is increased metabolic demand and insulin resistance is developed. This metabolic state increases the demand on beta-cells to augment insulin biosynthesis and release. In this respect, ERalpha is directly implicated in the E2-regulation of insulin content and secretion, while ERbeta is in the E2-potentiation of glucose-induced insulin release. Both receptors develop their actions within the physiological range of E2. In addition, the G protein-coupled estrogen receptor (GPER1/GPR30) seems to be implicated in the E2-regulation of stimulus-secretion coupling in the three cell types of the islet. The increased demand of insulin production for long time may lead to beta-cell stress and apoptosis. ERalpha, ERbeta and GPER1/GPR30 are involved in preventing beta-cell apoptosis, impeding the loss of critical beta-cell mass. Therefore, estrogen receptors may play an essential role in the adaptation of the pancreas to insulin resistant periods.

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Angel Nadal, Paloma Alonso-Magdalena, Sergi Soriano, Cristina Ripoll, Esther Fuentes, Ivan Quesada, Ana Belen Ropero. Role of estrogen receptors alpha, beta and GPER1/GPR30 in pancreatic beta-cells. Frontiers in Bioscience-Landmark. 2011. 16(1); 251-260.