4.5 Review

Minireview: Estrogenic Protection of beta-Cell Failure in Metabolic Diseases

期刊

ENDOCRINOLOGY
卷 151, 期 3, 页码 859-864

出版社

ENDOCRINE SOC
DOI: 10.1210/en.2009-1107

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资金

  1. National Institutes of Health [RO1 DK074970]
  2. Juvenile Diabetes Research Foundation [1-2006-837]
  3. March of Dimes [6-FY7-312]
  4. EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [P50HD044405] Funding Source: NIH RePORTER
  5. NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK074970] Funding Source: NIH RePORTER

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The prevalence of diabetes is lower in premenopausal women, especially diabetic syndromes with insulin deficiency, suggesting that the female hormone 17 beta-estradiol protects pancreatic beta-cell function. In classical rodent models of beta-cell failure, 17 beta-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. (Endocrinology 151: 859-864, 2010)

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