期刊
JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY
卷 176, 期 -, 页码 31-37出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jsbmb.2017.02.012
关键词
Estrogen; GPER; Metabolism; Diabetes; Inflammation; Insulin resistance; Obesity
资金
- National Institutes of Health (NIH) [R01 CA127731, CA163890, CA194496, DK074970, DK107444]
- Dialysis Clinic, Inc.
- UNM Comprehensive Cancer Center [P30 CA118100]
- NATIONAL CANCER INSTITUTE [R01CA127731, R01CA163890, R01CA194496, P30CA118100] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK074970, R01DK107444] Funding Source: NIH RePORTER
Metabolic homeostasis is differentially regulated in males and females. The lower incidence of obesity and associated diseases in pre-menopausal females points towards the beneficial role of the predominant estrogen,17 beta-estradiol (E2). The actions of E2 are elicited by nuclear and extra-nuclear estrogen receptor (ER)alpha and ER beta, as well as the G protein-coupled estrogen receptor (GPER, previously termed GPR30). The roles of GPER in the regulation of metabolism are only beginning to emerge and much remains unclear. The present review highlights recent advances implicating the importance of GPER in metabolic regulation. Assessment of the specific metabolic roles of GPER employing GPER-deficient mice and highly selective GPER-targeted pharmacological agents, agonist G-1 and antagonists G-15 and G36, is also presented. Evidence from in vitro and in vivo studies involving either GPER deficiency or selective activation suggests that GPER is involved in body weight regulation, glucose and lipid homeostasis as well as inflammation. The therapeutic potential of activating GPER signaling through selective ligands for the treatment of obesity and diabetes is also discussed. (C) 2017 Elsevier Ltd. All rights reserved.
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