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Publication : The sexually dimorphic role of adipose and adipocyte estrogen receptors in modulating adipose tissue expansion, inflammation, and fibrosis.

First Author  Davis KE Year  2013
Journal  Mol Metab Volume  2
Issue  3 Pages  227-42
PubMed ID  24049737 Mgi Jnum  J:223192
Mgi Id  MGI:5648180 Doi  10.1016/j.molmet.2013.05.006
Citation  Davis KE, et al. (2013) The sexually dimorphic role of adipose and adipocyte estrogen receptors in modulating adipose tissue expansion, inflammation, and fibrosis. Mol Metab 2(3):227-42
abstractText  Our data demonstrate that estrogens, estrogen receptor-alpha (ERalpha), and estrogen receptor-beta (ERbeta) regulate adipose tissue distribution, inflammation, fibrosis, and glucose homeostasis, by determining that alphaERKO mice have increased adipose tissue inflammation and fibrosis prior to obesity onset. Selective deletion of adipose tissue ERalpha in adult mice using a novel viral vector technology recapitulated the findings in the total body ERalpha null mice. Generation of a novel mouse model, lacking ERalpha specifically from adipocytes (AdipoERalpha), demonstrated increased markers of fibrosis and inflammation, especially in the males. Additionally, we found that the beneficial effects of estrogens on adipose tissue require adipocyte ERalpha. Lastly, we determined the role of ERbeta in regulating inflammation and fibrosis, by breeding the AdipoERalpha into the betaERKO background and found that in the absence of adipocyte ERalpha, ERbeta has a protective role. These data suggest that adipose tissue and adipocyte ERalpha protects against adiposity, inflammation, and fibrosis in both males and females.
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