Document Detail


p53-induced adipose tissue inflammation is critically involved in the development of insulin resistance in heart failure.
MedLine Citation:
PMID:  22225876     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Several clinical studies have shown that insulin resistance is prevalent among patients with heart failure, but the underlying mechanisms have not been fully elucidated. Here, we report a mechanism of insulin resistance associated with heart failure that involves upregulation of p53 in adipose tissue. We found that pressure overload markedly upregulated p53 expression in adipose tissue along with an increase of adipose tissue inflammation. Chronic pressure overload accelerated lipolysis in adipose tissue. In the presence of pressure overload, inhibition of lipolysis by sympathetic denervation significantly downregulated adipose p53 expression and inflammation, thereby improving insulin resistance. Likewise, disruption of p53 activation in adipose tissue attenuated inflammation and improved insulin resistance but also ameliorated cardiac dysfunction induced by chronic pressure overload. These results indicate that chronic pressure overload upregulates adipose tissue p53 by promoting lipolysis via the sympathetic nervous system, leading to an inflammatory response of adipose tissue and insulin resistance.
Authors:
Ippei Shimizu; Yohko Yoshida; Taro Katsuno; Kaoru Tateno; Sho Okada; Junji Moriya; Masataka Yokoyama; Aika Nojima; Takashi Ito; Rudolf Zechner; Issei Komuro; Yoshio Kobayashi; Tohru Minamino
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cell metabolism     Volume:  15     ISSN:  1932-7420     ISO Abbreviation:  Cell Metab.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2012-01-09     Completed Date:  2012-05-03     Revised Date:  2012-06-15    
Medline Journal Info:
Nlm Unique ID:  101233170     Medline TA:  Cell Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  51-64     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
Affiliation:
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / metabolism*
Animals
Cell Line
Heart Failure / complications,  metabolism*,  physiopathology
Humans
Inflammation / complications,  metabolism*,  pathology
Insulin Resistance*
Isoproterenol / pharmacology
Lipid Metabolism / drug effects
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Pressure
Sympathetic Nervous System / metabolism
Tumor Suppressor Protein p53 / antagonists & inhibitors,  genetics,  metabolism*
Up-Regulation
Chemical
Reg. No./Substance:
0/Tumor Suppressor Protein p53; 7683-59-2/Isoproterenol
Comments/Corrections
Erratum In:
Cell Metab. 2012 May 2;15(5):787

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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