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Papers In Press, published online ahead of print November 3, 2005
J. Lipid Res., doi:10.1194/jlr.M500378-JLR200
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Submitted on August 22, 2005
Revised on November 2, 2005
Accepted on November 2, 2005

A role for FXR and human FGF-19 in the repression of paraoxonase-1 gene expression by bile acids

Diana M. Shih, Heidi R. Kast-Woelbern, Jack Wong, Yu-Rong Xia, Peter A. Edwards, and Aldons J. Lusis

Division of Cardiology, Department of Medicine, UCLA, Los Angeles, CA 90095-1679

Corresponding Author: dshih{at}mednet.ucla.edu

Paraoxonase-1 (PON1), an enzyme that metabolizes organophosphate insecticides, is secreted by the liver and transported in the blood complexed to HDL. In humans and mice, low plasma levels of PON1 have been also linked to the development of atherosclerosis. We previously reported that hepatic Pon1 expression was decreased when C57BL/6J mice were fed a high fat, high cholesterol diet supplemented with cholic acid. In the current report we utilized wild-type and farnesoid X receptor (FXR) null mice to demonstrate that this repression is dependent upon cholic acid and FXR. PON1 mRNA levels were also repressed when HepG2 cells, derived from a human hepatoma, were incubated with natural or highly specific synthetic FXR agonists. In contrast, fibroblast growth factor-19 (FGF-19) mRNA levels were greatly induced by these same FXR agonists. Furthermore, treatment of HepG2 cells with recombinant human FGF-19 significantly decreased PON1 mRNA levels. Finally, deletion studies revealed that the proximal -230 bp to –96 bp region of the PON1 promoter contains regulatory element(s) necessary for promoter activity and bile acid repression. These data demonstrate that human PON1 expression is repressed by bile acids through the actions of FXR and FGF-19.


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