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PPAR Research
Volume 2008, Article ID 286249, 9 pages
Review Article

The Role of NF- B in PPAR -Mediated Hepatocarcinogenesis

1Graduate Center for Nutritional Sciences, University of Kentucky, Lexington, KY 40536, USA
2College of Health and Human Services, Western Kentucky University, Bowling Green, KY 42101, USA
3Applied Biosystems, Foster City, CA 94404, USA
4Division of Transplant Surgery, Kidney Disease Center, Medical College of Wisconsin, Milwaukee, WI 53226, USA
5Food and Drug Administration, CFSAN/OFAS/DFCN, College Park, MD 20740, USA
6Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, KY 40536, USA

Received 30 May 2008; Revised 3 October 2008; Accepted 3 November 2008

Academic Editor: Dipak Panigrahy

Copyright © 2008 Howard P. Glauert et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


In this review, the role of NF- B in the induction of hepatocarcinogenesis by peroxisome proliferators is examined. The administration of peroxisome proliferators for more than a three-day period leads to the activation of NF- B in the livers of rats and mice. On the other hand, peroxisome proliferator activated receptor- (PPAR ) activation in non-hepatic tissues can lead to the inhibition of NF- B activation. Several lines of evidence support the hypothesis that the activation of NF- B by peroxisome proliferators in the liver is mediated by oxidative stress. The role of NF- B in peroxisome proliferator-induced hepatocarcinogenesis has been examined using NF- B knockout models. Specifically, the induction of cell proliferation and the promotion of liver carcinogenesis are inhibited in mice lacking the p50 subunit of NF- B. Overall, the activation of NF- B appears to be important in the carcinogenic activity of peroxisome proliferators.