期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 16, 期 -, 页码 251-260出版社
BIOSCIENCE RESEARCH INST-BRI
DOI: 10.2741/3686
关键词
Insulin Secretion; Insulin Biosynthesis; Diabetes; Estrogen Receptors; GPR30; Review
资金
- Ministerio de Ciencia e Innovacion [BFU2008-01492, BFU2007-67607]
- Generalitat Valenciana
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.
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