Role of estrogen receptors alpha, beta and GPER1/GPR30 in pancreatic beta-cells

Front Biosci (Landmark Ed). 2011 Jan 1;16:251-60. doi: 10.2741/3686.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Blood Glucose / metabolism
  • Endocrine Disruptors / pharmacology
  • Estrogen Receptor alpha / physiology*
  • Estrogen Receptor beta / physiology*
  • Homeostasis
  • Humans
  • Insulin / biosynthesis
  • Insulin / metabolism
  • Insulin Secretion
  • Insulin-Secreting Cells / physiology*
  • Mice
  • Receptors, Estrogen
  • Receptors, G-Protein-Coupled / physiology*

Substances

  • Blood Glucose
  • Endocrine Disruptors
  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • GPER1 protein, human
  • GPER1 protein, mouse
  • Insulin
  • Receptors, Estrogen
  • Receptors, G-Protein-Coupled