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Adv Exp Med Biol. 2017;1043:385-399. doi: 10.1007/978-3-319-70178-3_18.

The Role of Estrogens in Pancreatic Islet Physiopathology.

Author information

1
Department of Medicine, Section of Endocrinology and Metabolism, Tulane University Health Sciences Center, School of Medicine, New Orleans, LA, USA. fmauvais@tulane.edu.
2
L'institut du Thorax, INSERM-CNRS, University of Nantes, Nantes, France.
3
Diabetes, Endocrinology, and Obesity Branch, NIDDK, Bethesda, MD, USA.
4
Xiamen Diabetes Institute, the First Affiliated Hospital of Xiamen University, Xiamen, China.
5
Department of Pediatric, Emory University School of Medicine, Atlanta, GA, USA.
6
Department of Food and Biotechnology, Korea University, Sejong, South Korea.

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.

PMID:
29224104
DOI:
10.1007/978-3-319-70178-3_18
[Indexed for MEDLINE]

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