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(The FASEB Journal. 1998;12:1341-1348.)
© 1998 FASEB

RESEARCH COMMUNICATION

Rapid insulinotropic effect of 17ß-estradiol via a plasma membrane receptor

Angel Nadala,1, Juan M. Roviraa, Ouahiba Laribia, Trinidad Leon-quintoa, Etelvina Andreua, Cristina Ripolla, and Bernat Soriaa

a Institute of Bioengineering and Department of Physiology, Miguel Hernández University, San Juan Campus, Alicante, Spain

Impaired insulin secretion is a hallmark in both type I and type II diabetic individuals. Whereas type I (insulin-dependent diabetes mellitus) implies ß-cell destruction, type II (non-insulin dependent diabetes mellitus), responsible for 75% of diabetic syndromes, involves diminished glucose-dependent secretion of insulin from pancreatic ß-cells. Although a clear demonstration of a direct effect of 17ß-estradiol on the pancreatic ß-cell is lacking, an in vivo insulinotropic effect has been suggested. In this report we describe the effects of 17ß-estradiol in mouse pancreatic ß-cells. 17ß-Estradiol, at physiological concentrations, closes KATP channels, which are also targets for antidiabetic sulfonylureas, in a rapid and reversible manner. Furthermore, in synergy with glucose, 17ß-estradiol depolarizes the plasma membrane, eliciting electrical activity and intracellular calcium signals, which in turn enhance insulin secretion. These effects occur through a receptor located at the plasma membrane, distinct from the classic cytosolic estrogen receptor. Specific competitive binding and localization of 17ß-estradiol receptors at the plasma membrane was demonstrated using confocal reflective microscopy and immunocytochemistry. Gaining deeper knowledge of the effect induced by 17ß-estradiol may be important in order to better understand the hormonal regulation of insulin secretion and for the treatment of NIDDM.—Nadal, A., Rovira, J. M., Laribi, O., Leon-Quinto, T., Andreu, E., Ripoll, C., Soria, B. Rapid insulinotropic effect of 17ß-estradiol via a plasma membrane receptor. FASEB J. 12, 1341–1348 (1998)


Key Words: intracellular calcium • KATP channels • insulin secretion • confocal microscopy • membrane estrogen receptor.




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