Role of ER¦Â and GPR30 in the endocrine pancreas: A matter of estrogen dose
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- 作者：Ana B. Ropero ; Yefei Pang ; Paloma Alonso-Magdalena ; Peter Thomas ; ¨¢ngel Nadal
- 关键词：GPR30 ; GPER ; Estrogen receptor ¦Á ; Estrogen receptor ¦Â ; Glucose tolerance ; Glycemia ; Insulin ; Insulin resistance ; Islets of Langerhans
- 刊名：Steroids
- 出版年：2012
- 出版时间：August, 2012
- 年：2012
- 卷：77
- 期：10
- 页码：951-958
- 全文大小：619 K
文摘
The endocrine pancreas has emerged as a target for estrogens. The functions of pancreatic ¦Á-, ¦Â- and ¦Ä-cells are modulated by the endogenous hormone, 17¦Â-estradiol (E2). Low physiological concentrations (100 pM-1 nM) of E2 rapidly decrease the activity of the ATP-sensitive potassium channel (KATP) and enhance glucose-induced insulin release in ¦Â-cells in an estrogen receptor ¦Â (ER¦Â)-dependent manner. In addition to the insulinotropic action of ER¦Â, the newly described estrogen receptor, GPR30, is involved in the insulinotropic effects of high doses of E2 (100 nM-5 ¦ÌM). The specific GPR30 agonist G1 also increases insulin secretion in ¦Â-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.