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c-Jun N-terminal kinase is involved in the suppression of adiponectin expression by TNF-alpha in 3T3-L1 adipocytes

Authors
Kim, KKim, JKJeon, JHYoon, SRChoi, IYang, Y
Issue Date
Feb-2005
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
adiponectin; JNK; 3T3-L1 adipocytes; PPAR-gamma
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.327, no.2, pp 460 - 467
Pages
8
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
327
Number
2
Start Page
460
End Page
467
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/148817
DOI
10.1016/j.bbrc.2004.12.026
ISSN
0006-291X
1090-2104
Abstract
Adiponectin, one of adipokines that is secreted from adipocytes, plays an important role in the regulation of glucose and lipid metabolism. Paradoxically, serum concentrations of adiponectin are decreased in obese and type 2 diabetic patients, although it is produced in adipose tissue. On the other hand, plasma TNF-alpha levels are increased in such subjects. In the present study, the mechanism by which adiponectin is regulated by TNF-alpha was investigated. The decreased adiponectin mRNA levels by TNF-a were partially recovered by treatment with a c-Jun N-terminal kinase (JNK) inhibitor or the PPAR-gamma agonist rosiglitazone in 3T3-L1 adipocytes. Interestingly, however, cotreatment with the JNK inhibitor and rosiglitazone led to a recovery of TNF-alpha-mediated adiponectin suppression to the control level. The JNK inhibitor regulated the expression of adiponectin by the increase of PPAR-gamma DNA binding activity and the recovery of its mRNA expression while rosiglitazone acted via a PPAR-gamma independent pathway which remains to be elucidated. These findings suggest that the JNK signaling pathway, activated by TNF-alpha, is involved in the regulation of adiponectin expression. (C) 2004 Elsevier Inc. All rights reserved.
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