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A more recent version of this article appeared on June 1, 2005

Papers In Press, published online ahead of print March 16, 2005
J. Lipid Res., doi:10.1194/jlr.C500007-JLR200
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Submitted on February 17, 2005
Revised on March 16, 2005
Accepted on March 9, 2005

Triglyceride-rich lipoprotein metabolism in unique VLDL receptor, LDL receptor, and LRP triple-deficient mice

Sonia M. S. Espirito Santo, Patrick C. N. Rensen, Jeltje R. Goudriaan, André Bensadoun, Niels Bovenschen, Peter J. Voshol, Louis M. Havekes, and Bart J. M. Van Vlijmen

Department of Endocrinology and Metabolism, Leiden University Medical Center, Leiden, Zuid-Holland 2300 RC

Corresponding Author: P.C.N.Rensen{at}lumc.nl

The VLDL receptor (VLDLR), LDL receptor (LDLR), and LRP are the three main apoE-recognizing endocytic receptors involved in the clearance of triglyceride (TG)-rich lipoproteins from plasma. Whereas LDLR-deficiency in mice results in accumulation of plasma LDL-sized lipoproteins, VLDLR or LRP deficiency alone only minimally affect plasma lipoproteins. To investigate the combined effect of the absence of these receptors on TG-rich lipoprotein levels, we now generated unique VLDLR, LDLR, and LRP triple-deficient mice. As compared with wild-type mice, these mice markedly accumulated plasma lipids and lipases. These mice did not show aggravated hyperlipidemia as compared with LDLR and LRP double-deficient mice, but plasma TG was elevated after high-fat diet feeding. In addition, these mice showed a severely decreased postprandial TG clearance typical of VLDLR-deficient mice. Collectively, although VLDLR-deficiency in LRP and LDLR-deficient mice does not aggravate hyperlipidemia, these triple-deficient mice represent a unique model of markedly delayed TG clearance on a hyperlipidemic background.


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