title: Role of estrogen receptors alpha, beta and GPER1/GPR30 in pancreatic beta-cells.
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.
authors.affiliation: CIBER de Diabetes y Enfermedades Metabolicas Asociadas and Instituto de Bioingenieria, Universidad Miguel Hernandez de Elche, Elche, Spain. nadal@umh.es
authors.forename: Angel
authors.initials: A
authors.lastname: Nadal
authors.forename: Paloma
authors.initials: P
authors.lastname: Alonso-Magdalena
authors.forename: Sergi
authors.initials: S
authors.lastname: Soriano
authors.forename: Cristina
authors.initials: C
authors.lastname: Ripoll
authors.forename: Esther
authors.initials: E
authors.lastname: Fuentes
authors.forename: Ivan
authors.initials: I
authors.lastname: Quesada
authors.forename: Ana Belen
authors.initials: AB
authors.lastname: Ropero
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D052244:Endocrine Disruptors / Q000494:pharmacology; D047628:Estrogen Receptor alpha / Q000502:physiology*; D047629:Estrogen Receptor beta / Q000502:physiology*; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000096:biosynthesis / Q000378:metabolism; D000078790:Insulin Secretion; D050417:Insulin-Secreting Cells / Q000502:physiology*; D051379:Mice; D011960:Receptors, Estrogen; D043562:Receptors, G-Protein-Coupled / Q000502:physiology*
chemical_list: D001786:Blood Glucose; D052244:Endocrine Disruptors; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; C109584:GPER1 protein, human; C532507:GPER1 protein, mouse; D007328:Insulin; D011960:Receptors, Estrogen; D043562:Receptors, G-Protein-Coupled