Role of ERβ and GPR30 in the endocrine pancreas: A matter of estrogen dose

Steroids. 2012 Aug;77(10):951-8. doi: 10.1016/j.steroids.2012.01.015. Epub 2012 Jan 28.

Abstract

The endocrine pancreas has emerged as a target for estrogens. The functions of pancreatic α-, β- and δ-cells are modulated by the endogenous hormone, 17β-estradiol (E2). Low physiological concentrations (100pM-1nM) of E2 rapidly decrease the activity of the ATP-sensitive potassium channel (K(ATP)) and enhance glucose-induced insulin release in β-cells in an estrogen receptor β (ERβ)-dependent manner. In addition to the insulinotropic action of ERβ, the newly described estrogen receptor, GPR30, is involved in the insulinotropic effects of high doses of E2 (100nM-5μM). The specific GPR30 agonist G1 also increases insulin secretion in β-cells. Low glucose-induced calcium oscillations and glucagon secretion are suppressed by E2. The effects on glucagon secretion may be mediated by GPR30. Somatostatin release is also decreased by E2 and G1. In this review we summarize all the data published up to date on the rapid insulinotropic effects of estrogens in the endocrine pancreas and propose a model to integrate the estrogen actions mediated through both receptors.

Publication types

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

MeSH terms

  • Animals
  • Estradiol / pharmacology
  • Estradiol / physiology*
  • Estrogen Receptor alpha / metabolism
  • Estrogen Receptor alpha / physiology
  • Estrogen Receptor beta / metabolism
  • Estrogen Receptor beta / physiology*
  • Estrogens / pharmacology
  • Estrogens / physiology*
  • Glucose / metabolism
  • Humans
  • Insulin / metabolism
  • Insulin Secretion
  • Islets of Langerhans / cytology
  • Islets of Langerhans / metabolism*
  • Receptors, Estrogen / metabolism
  • Receptors, Estrogen / physiology*
  • Receptors, G-Protein-Coupled / metabolism
  • Receptors, G-Protein-Coupled / physiology*

Substances

  • Estrogen Receptor alpha
  • Estrogen Receptor beta
  • Estrogens
  • GPER1 protein, human
  • Insulin
  • Receptors, Estrogen
  • Receptors, G-Protein-Coupled
  • Estradiol
  • Glucose