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A more recent version of this article appeared on March 1, 2004

Papers In Press, published online ahead of print December 16, 2003
J. Lipid Res., doi:10.1194/jlr.M300432-JLR200
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Submitted on October 20, 2003
Revised on December 1, 2003
Accepted on December 15, 2003

Cholesteryl ester transfer protein modulates the effect of liver X receptor agonists on cholesterol transport and excretion in the mouse

David Masson, Bart Staels, Thomas Gautier, Catherine Desrumaux, Anne Athias, Naig Le Guern, Martina Schneider, Zoulika Zak, Laure Dumont, Valerie Deckert, Alan Tall, Xian-Cheng Jiang, and Laurent Lagrost

Biochemistry, INSERM U498, Dijon 21034

Corresponding Author: david.masson{at}laposte.net

Abstract Background&aims: Human plasma, unlike mouse plasma contains the cholesteryl ester transfer protein (CETP) that may influence the transport of cholesterol from peripheral tissues to the liver, and its biliary excretion. Liver X receptor (LXR), an oxysterol-activated nuclear receptor induces CETP transcription via a direct repeat (DR) 4 element in the CETP gene promoter. The aim of the study was to assess in vivo the impact of LXR activation on hepatic CETP expression and its consequences in terms of plasma lipid metabolism, hepatic lipid content and biliary cholesterol secretion . Methods: Wild type and humanized mice expressing human CETP under the control of its natural flanking regions were treated for five days with T0901317 LXR agonist. Results: Short-term treatment with the T0901317 LXR agonist produced marked rises in both hepatic CETP mRNA and plasma CETP activity levels (8- and 3-fold, respectively). Interestingly, the LXR agonist-mediated, 2-fold rise in both total and HDL cholesterol levels in treated wild-type mice was not observed in mice expressing human CETP. Whereas liver triglycerides were increased to similar extents in both wild-type and CETPTg mice treated with T0901317, the CETP-mediated accumulation of cholesterol in the liver of CETPTg mice was fully reversed by administration of the LXR agonist. Moreover, LXR activation induced a 2-fold increase in the hepatic LDL-receptor gene expression in both wild-type and CETPTg mice, and it produced a significantly greater rise in biliary cholesterol secretion in CETPTg mice as compared to wild-type mice. Conclusions: The LXR-mediated upregulation of CETP, in conjunction with other proteins involved in reverse cholesterol transport, constitutes a major determinant of the effect of LXR agonist on biliary secretion of cholesterol.


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