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A more recent version of this article appeared on October 1, 2005

Papers In Press, published online ahead of print August 1, 2005
J. Lipid Res., doi:10.1194/jlr.M500217-JLR200
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Submitted on May 27, 2005
Accepted on July 26, 2005

Suppression of estrogen-related receptor-alpha and medium-chain acyl coenzyme A dehydrogenase in the acute phase response

Min Sun Kim, Judy K. Shigenaga, Arthur H. Moser, Kenneth R. Feingold, and Carl Grunfeld

Metabolism Section/Medicine, University of California, San Francisco, San Francisco, CA 94121

Corresponding Author: grunfld{at}itsa.ucsf.edu

Fatty acid oxidation provides energy in tissues with high metabolic demands. During the acute phase response (APR) induced by infection and inflammation, fatty acid oxidation is decreased associated with hypertriglyceridemia. Little is known about the mechanism by which the APR decreases fatty acid oxidation. Therefore, we investigated whether the APR affects the expression of medium-chain acyl CoA dehydrogenase (MCAD), its regulator the estrogen-related receptor a (ERRa) and a key coactivator of ERRa, the peroxisome proliferator-activated receptor  coactivator-1a (PGC-1a). mRNA levels of PGC-1a, ERRa and MCAD are markedly reduced in the liver, heart and kidney of mice during the LPS-induced APR. The decreases were rapid and occurred at very low doses of LPS. MCAD activity in liver was also reduced. Furthermore, binding of hepatic nuclear extracts to the ERRa-response element found in the promoter region of MCAD was significantly decreased during the APR, suggesting the decreased transcription of the MCAD gene. The binding activity was identified as ERRa by supershift with antibody to ERRa. Similar decreases in mRNA levels of these genes occur during zymosan and turpentine induced inflammation, indicating that suppression of PGC-1a, ERRa, and MCAD pathway is a general response during infection and inflammation. Our study provides a potential mechanism by which the APR decreases fatty acid oxidation.


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