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Originally published In Press as doi:10.1194/jlr.M600205-JLR200 on October 19, 2006

Papers In Press, published online ahead of print January 1, 2007
J. Lipid Res., doi:10.1194/jlr.M600205-JLR200
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Journal of Lipid Research, Vol. 48, 30-40, January 2007
Copyright © 2007 by American Society for Biochemistry and Molecular Biology

Hepatic lipid accumulation in apolipoprotein C-I-deficient mice is potentiated by cholesteryl ester transfer proteinboxs

Thomas Gautier1,*, Uwe J. F. Tietge*, Renze Boverhof*, Frank G. Perton*, Naig Le Guern{dagger}, David Masson{dagger}, Patrick C. N. Rensen§,**, Louis M. Havekes§,**, Laurent Lagrost{dagger} and Folkert Kuipers*

* Center for Liver, Digestive, and Metabolic Diseases, Department of Pediatrics, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands
{dagger} Biochimie des Lipoprotéines, INSERM U498, Faculté de Médecine, 7 boulevard Jeanne d'Arc, 21079 Dijon, France
§ Netherlands Organization for Applied Scientific Research-Quality of Life, Gaubius Laboratory, P.O. Box 2215, 2301 CE Leiden, The Netherlands
** Departments of General Internal Medicine, Endocrinology and Metabolic Diseases, and Cardiology, Leiden University Medical Center, P.O. Box 9600, 2300 RC Leiden, The Netherlands

boxs The online version of this article (available at http://www.jlr.org) contains supplementary data in the form of a table.

Published, JLR Papers in Press, October 19, 2006.

1 To whom correspondence should be addressed. e-mail: t.gautier{at}med.umcg.nl

The impact of apolipoprotein C-I (apoC-I) deficiency on hepatic lipid metabolism was addressed in mice in the presence or the absence of cholesteryl ester transfer protein (CETP). In addition to the expected moderate reduction in plasma cholesterol levels, apoCIKO mice showed significant increases in the hepatic content of cholesteryl esters (+58%) and triglycerides (+118%) and in biliary cholesterol concentration (+35%) as compared with wild-type mice. In the presence of CETP, hepatic alterations resulting from apoC-I deficiency were enforced, with up to 58% and 302% increases in hepatic levels of cholesteryl esters and triglycerides in CETPTg/apoCIKO mice versus CETPTg mice, respectively. Biliary levels of cholesterol, phospholipids, and bile acids were increased by 88, 77, and 20%, respectively, whereas total cholesterol, HDL cholesterol, and triglyceride concentrations in plasma were further reduced in CETPTg/apoCIKO mice versus CETPTg mice. Finally, apoC-I deficiency was not associated with altered VLDL production rate. In line with the previously recognized inhibition of lipoprotein clearance by apoC-I, apoC-I deficiency led to decreased plasma lipid concentration, hepatic lipid accumulation, and increased biliary excretion of cholesterol. The effect was even greater when the alternate reverse cholesterol transport pathway via VLDL/LDL was boosted in the presence of CETP.

Supplementary key words liver • bile • cholesterol • triglycerides

Abbreviations: ABCB4, ATP binding cassette B4; ALAT, alanine transaminase; apoC-I, apolipoprotein C-I; ASAT, aspartate transaminase; CETP, cholesteryl ester transfer protein; LPL, lipoprotein lipase; NBD-CE, nitrobenzoxadiazole-labeled cholesteryl esters


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