Minireview: Estrogenic protection of beta-cell failure in metabolic diseases.
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.
Liu
Suhuan
S
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.
Mauvais-Jarvis
Franck
F
D000818:Animals; D002470:Cell Survival; D004967:Estrogens / Q000502:physiology*; D006801:Humans; D050417:Insulin-Secreting Cells / Q000502:physiology*; D011960:Receptors, Estrogen / Q000502:physiology*; D012727:Sex Characteristics
D004967:Estrogens; D011960:Receptors, Estrogen