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A more recent version of this article appeared on December 1, 2006

Papers In Press, published online ahead of print September 6, 2006
J. Lipid Res., doi:10.1194/jlr.M600140-JLR200
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Submitted on March 24, 2006
Revised on September 6, 2006
Accepted on September 6, 2006

Upregulation of liver VLDL receptor and FAT/CD36 expressions in LDLR-/- apoB100/100 mice fed trans-10,cis-12 conjugated linoleic acid

Pascal Degrace, Bastien Moindrot, Ismaël Mohamed, Joseph Gresti, Zhen-Yu Du, Jean-Michel Chardigny, Jean-Louis Sébédio, and Pierre Clouet

UPRES Lipides et Nutrition, Université de Bourgogne, DIJON 21000

Corresponding Author: pascal.degrace{at}u-bourgogne.fr

The present study explores the mechanisms responsible for the fatty liver setup in mice fed trans-10,cis-12-C18:2 (t10c12 CLA) hypothesizing that an induction of LDL receptor (LDLR) expression is associated to lipid accumulation. In this goal, the effects of t10c12CLA treatment on lipid parameters, serum lipoproteins and expression of liver lipid receptors were measured in LDLR-/- apoB100/100 mice, as a model of human familial hypercholesterolemia itself LDLR-depleted. Mice were fed t10c12 CLA over 2 or 4 weeks. We first observed that the treatment still induced a liver steatosis, even in the absence of LDLR. Mice treated for 2 weeks exhibited a hypertriglyceridemia with high levels of VLDL and HDL, whereas a 4-week treatment inversely induced a reduction of serum triglycerides essentially through a decrease in VLDL levels. In the absence of LDLR, the mRNA levels of other proteins such as VLDL receptor, lipoprotein lipase and fatty acid translocase (FAT/CD36), usually not expressed in the liver, were upregulated suggesting their involvement in the steatosis setup and the lipoprotein clearance. Data also suggest that the triglyceride lowering effect induced by t10c12 CLA treatment was due both to the reduction of circulating free fatty acids consecutive to the severe lipoatrophy and to the high capacities of liver to clear off plasma lipids.


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