Department 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.
Endocrinology. 2010 Mar;151(3):859-64. doi: 10.1210/en.2009-1107. Epub 2009 Dec 4.
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.
绝经前女性的糖尿病患病率较低，尤其是胰岛素缺乏的糖尿病综合征，这表明女性激素 17β-雌二醇能保护胰岛β细胞的功能。在经典的胰岛β细胞衰竭啮齿动物模型中，生理浓度的 17β-雌二醇可保护胰岛β细胞免受脂毒性、氧化应激和细胞凋亡的影响。在这篇综述中，我们整合了证据表明雌激素及其受体对胰岛生物学有直接影响。雌激素受体 (ER)-α、ER-β 和 G 蛋白偶联 ER 存在于β细胞中，并增强胰岛的存活。它们还改善胰岛的脂质稳态和胰岛素生物合成。我们还讨论了 ER 调节胰岛素敏感性和能量稳态的证据，这在糖尿病和肥胖条件下间接改变了β细胞的生物学。
