Endocrine Abstracts (2010) 22 S25.2

Non-classical actions of estrogens in endocrine pancreas

Sergi Soriano1, Ana Ropero1, Paloma Alonso-Magdalena1, Cristina Ripoll1, Esther Fuentes1, Ivan Quesada1, Birgit Gassner2, Michaela Kuhn2, Jan-Ake Gustafsson3,4 & Angel Nadal1

1Instituto Bioingeniería and CIBERDEM, Universidad Miguel Hernández de Elche, Elche, Spain; 2Institute of Physiology, University of Würzburg, Würzburg, Germany; 3Department of Biosciences and Nutrition, Huddinge, Sweden; 4Center for Nuclear Receptors and Cell Signaling, University of Houston, Houston, Texas, USA.

The estrogen receptors ERα and ERβ are currently considered important molecules in glucose and lipid metabolism, although their specific roles in pancreatic β-cells are still greatly unknown.

The function of pancreatic β-cells is the biosynthesis and release of insulin, the only hormone able to decrease blood glucose levels. It has been recently described that ERα plays an essential role in the regulation of insulin biosynthesis by 17β-estradiol, contributing to an enhancement of glucose-induced insulin secretion (Alonso-Magdalena et al. 2008). In addition, 17β-estradiol rapidly (in min) decreases KATP channel activity and increases insulin release in a cGMP dependent manner (Nadal et al. 1998, Ropero et al. 1999). The 17β-estradiol-induced reduction of KATP channel activity is mimicked by the ERβ agonist, DPN; this action is missing in β-cells from ERβ knock-out mice (βERKO). Both the blockade of KATP channels and the release of insulin are abolished in β-cells obtained for guanylyl cyclase A knock out mice (GC-A KO). Therefore, evidence indicate that the estrogen receptor ERβ and the guanylyl cyclase-A receptor (GC-A) are involved in the 17β-estradiol triggered action in β-cells (Soriano et al. 2009). These results may be relevant to clarify the role of estrogen receptors in the endocrine pancreas adaptation to pregnancy and point to ERβ agonists as effective insulinotropic agents.

Alonso-Magdalena et al. PloS ONE 2008 3 e2069.

Nadal et al. FASEB J 1998 521 397–407.

Ropero et al. J Physiol 1999 12 1341–1348.

Soriano et al. Mol Endocrinol 2009 23.

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