Abstract
In rodent models of insulin-deficient diabetes, 17β-estradiol (E2) protects pancreatic insulin-producing β-cells against oxidative stress, amyloid polypeptide toxicity, gluco-lipotoxicity, and apoptosis. Three estrogen receptors (ERs)-ERα, ERβ, and the G protein-coupled ER (GPER)-have been identified in rodent and human β-cells. This chapter describes recent advances in our understanding of the role of ERs in islet β-cell function, nutrient homeostasis, survival from pro-apoptotic stimuli, and proliferation. We discuss why and how ERs represent potential therapeutic targets for the maintenance of functional β-cell mass.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Animals
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Apoptosis
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Blood Glucose / metabolism
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Cell Proliferation
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Diabetes Mellitus, Experimental / metabolism
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Diabetes Mellitus, Experimental / pathology
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Diabetes Mellitus, Experimental / physiopathology
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Diabetes Mellitus, Type 1 / metabolism*
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Diabetes Mellitus, Type 1 / pathology
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Diabetes Mellitus, Type 1 / physiopathology
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Diabetes Mellitus, Type 1 / therapy
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Estradiol / adverse effects
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Estrogen Replacement Therapy* / adverse effects
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Estrogens / adverse effects
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Estrogens / metabolism*
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Humans
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Hypoglycemic Agents / therapeutic use
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Insulin / metabolism*
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Insulin Secretion
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Islets of Langerhans / metabolism*
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Islets of Langerhans / pathology
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Islets of Langerhans / physiopathology
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Islets of Langerhans / surgery
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Islets of Langerhans Transplantation
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Ligands
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Mice, Inbred NOD
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Nutritional Status
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Receptors, Estrogen / drug effects
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Receptors, Estrogen / metabolism*
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Risk Factors
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Signal Transduction
Substances
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Blood Glucose
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Estrogens
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Hypoglycemic Agents
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Insulin
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Ligands
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Receptors, Estrogen
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Estradiol