Abstract
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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