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Publication
P65 inactivation in adipocytes and macrophages attenuates adipose inflammatory
response in lean but not in obese mice.
Authors Gao Z, Zhang J, Henagan TM, Lee JH, Ye X, Wang H, Ye J
Submitted By Submitted Externally on 8/8/2017
Status Published
Journal American journal of physiology. Endocrinology and metabolism
Year 2015
Date Published 3/15/2015
Volume : Pages 308 : E496 - 505
PubMed Reference 25564477
Abstract NF-?B induces transcriptional expression of proinflammatory genes and
antiapoptotic genes. The two activities of NF-?B remain to be characterized in
the mechanism of chronic inflammation in obesity. To address this issue, we
inactivated NF-?B in adipose tissue by knocking out p65 (RelA) in mice
(F-p65-KO) and examined the inflammation in lean and obese conditions. In the
lean condition, KO mice exhibited a reduced inflammation in adipose tissue with
a decrease in macrophage infiltration, M1 polarization, and proinflammatory
cytokine expression. In the obese condition, KO mice had elevated inflammation
with more macrophage infiltration, M1 polarization, and cytokine expression. In
the mechanism of enhanced inflammation, adipocytes and macrophages exhibited an
increase in cellular apoptosis, which was observed with more formation of
crown-like structures (CLS) in fat tissue of KO mice. Body weight, glucose
metabolism, and insulin sensitivity were not significantly altered in KO mice
under the lean and obese conditions. A modest but significant reduction in body
fat mass was observed in KO mice on HFD with an elevation in energy expenditure.
The data suggest that in the control of adipose inflammation, NF-?B exhibits
different activities in the lean vs. obese condition. NF-?B is required for
expression of proinflammatory genes in the lean but not in the obese condition.
NF-?B is required for inhibition of apoptosis in the obese condition, in which
proinflammation is enhanced by NF-?B inactivation.




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