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Endotoxin, zymosan, and cytokines decrease the expression of the transcription factor, carbohydrate response element
Kenneth R Feingold1, Judy K Shigenaga, Sophie M Patzek
1Metabolism Section, Department of Veterans Affairs Medical Center, University of California-San Francisco, 4150 Clement Street, San Francisco, CA 94121, USA. kenneth.feingold@ucsf.edu
Innate Immunity
|January 27, 2010
Summary
Lipopolysaccharide (LPS) and inflammatory stimuli rapidly decrease carbohydrate response element binding protein (ChREBP) levels in mice. This down-regulation impacts ChREBP target genes, highlighting ChREBP
Area of Science:
- Metabolism
- Molecular Biology
- Immunology
Background:
- Carbohydrate response element binding protein (ChREBP) regulates glucose metabolism genes.
- ChREBP activity increases with glucose, promoting lipogenesis.
- The regulation of ChREBP during inflammatory states is not well understood.
Purpose of the Study:
- To investigate the effect of inflammatory stimuli on ChREBP expression and activity.
- To determine if ChREBP is regulated during the acute phase response.
- To identify tissues where ChREBP expression is affected by inflammation.
Main Methods:
- Mice were treated with lipopolysaccharide (LPS), zymosan, or turpentine.
- Hepatic ChREBP mRNA and protein levels were measured.
- Expression of ChREBP target genes was analyzed.
- In vitro studies used Hep3B cells treated with TNF-α and IL-1β.
Main Results:
- LPS treatment caused a rapid and dose-dependent decrease in hepatic ChREBP mRNA and protein.
- Zymosan and turpentine also reduced liver ChREBP levels and target gene expression.
- Pro-inflammatory cytokines TNF-α and IL-1β decreased ChREBP expression in vivo and in vitro.
- ChREBP expression was also reduced in muscle and adipose tissue following LPS treatment.
Conclusions:
- ChREBP is significantly down-regulated during the acute phase response induced by inflammatory stimuli.
- This down-regulation affects the expression of key metabolic genes regulated by ChREBP.
- ChREBP is identified as a transcription factor regulated during acute inflammation.
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