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Endocrinology. 2010 Mar;151(3):859-64. doi: 10.1210/en.2009-1107. Epub 2009 Dec 4.

Minireview: Estrogenic protection of beta-cell failure in metabolic diseases.

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  • 1Department of Medicine, Division of Endocrinology, Metabolism, and Molecular Medicine, Northwestern University, Feinberg School of Medicine, 303 East Chicago Avenue, Tarry 15-761, Chicago, Illinois 60611, USA.

Erratum in

  • Endocrinology. 2010 Sep;151(9):4597.


The prevalence of diabetes is lower in premenopausal women, especially diabetic syndromes with insulin deficiency, suggesting that the female hormone 17beta-estradiol protects pancreatic beta-cell function. In classical rodent models of beta-cell failure, 17beta-estradiol at physiological concentrations protects pancreatic beta-cells against lipotoxicity, oxidative stress, and apoptosis. In this review, we integrate evidence showing that estrogens and their receptors have direct effects on islet biology. The estrogen receptor (ER)-alpha, ER beta, and the G-protein coupled ER are present in beta-cells and enhance islet survival. They also improve islet lipid homeostasis and insulin biosynthesis. We also discuss evidence that ERs modulate insulin sensitivity and energy homeostasis, which indirectly alter beta-cell biology in diabetic and obese conditions.

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