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Fuente-Martin, E. ; García-Cáceres, C. ; Morselli, E.* ; Clegg, D.J.* ; Chowen, J.A.* ; Finan, B. ; Brinton, R.D.* ; Tschöp, M.H.

Estrogen, astrocytes and the neuroendocrine control of metabolism.

Rev. Endocr. Metab. Disord. 14, 331-338 (2013)
Verlagsversion Volltext DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Obesity, and its associated comorbidities such as type 2 diabetes, cardiovascular diseases, and certain cancers, represent major health challenges. Importantly, there is a sexual dimorphism with respect to the prevalence of obesity and its associated metabolic diseases, implicating a role for gonadal hormones. Specifically, estrogens have been demonstrated to regulate metabolism perhaps by acting as a leptin mimetic in the central nervous system (CNS). CNS estrogen receptors (ERs) include ER alpha (ERα) and ER beta (ERβ), which are found in nuclear, cytoplasmic and membrane sites throughout the brain. Additionally, estrogens can bind to and activate a G protein-coupled estrogen receptor (GPER), which is a membrane-associated ER. ERs are expressed on neurons as well as glia, which are known to play a major role in providing nutrient supply for neurons and have recently received increasing attention for their potentially important involvement in the CNS regulation of systemic metabolism and energy balance. This brief overview summarizes data focusing on the potential role of astrocytic estrogen action as a key component of estrogenic modulation responsible for mediating the sexual dimorphism in body weight regulation and obesity.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Review
Korrespondenzautor
Schlagwörter Obesity; Sexual dimorphism; Estrogens; Leptin; Astrocates; Central-nervous-system ; Intracellular Calcium-release ; Body-fat Distribution ; Leptin Receptor Gene ; Sex Steroid-hormones ; Food-intake ; Hypothalamic Astrocytes ; Energy Homeostasis ; Arcuate Nucleus ; Glial-cells
ISSN (print) / ISBN 1389-9155
e-ISSN 1573-2606
Quellenangaben Band: 14, Heft: 4, Seiten: 331-338 Artikelnummer: , Supplement: ,
Verlag Springer
Verlagsort Boston
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed