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Originally published In Press as doi:10.1074/jbc.M106396200 on August 23, 2001

J. Biol. Chem., Vol. 276, Issue 44, 40693-40697, November 2, 2001
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Stimulation of the in Vivo Production of Very Low Density Lipoproteins by Apolipoprotein E Is Independent of the Presence of the Low Density Lipoprotein Receptor*

Bas TeusinkDagger §, Arjen R. Mensenkamp, Hans van der BoomDagger , Folkert Kuipers, Ko Willems van Dijk||, and Louis M. HavekesDagger **Dagger Dagger

From the Dagger  TNO Prevention and Health, Gaubius Laboratory, NL-2301 CE Leiden, The Netherlands,  Center for Liver, Digestive and Metabolic Diseases, Laboratory of Pediatrics, University Hospital Groningen, 9713 GZ Groningen, The Netherlands, and Departments of || Human and Clinical Genetics, ** Cardiology, and Dagger Dagger  Internal Medicine, Leiden University Medical Center, 2300 RA Leiden, The Netherlands

Apolipoprotein (apo) E stimulates the secretion of very low density lipoproteins (VLDLs) by an as yet unknown mechanism. Recently, a working mechanism for apoE was proposed (Twisk, J., Gillian-Daniel, D. L., Tebon, A., Wang, L., Barrett, P. H., and Attie, A. D. (2000) J. Clin. Invest. 105, 521-532) in which apoE prevents the inhibitory action of the low density lipoprotein receptor (LDLr) by binding to it. We have first tested whether this newly described effect of the LDLr on VLDL secretion, obtained in vitro, is also observed in vivo. In LDLr knockout mice (LDLr-/-), the production of VLDL triglycerides and apoB was 30% higher than that in controls. Also the ratio of apoB100:apoB48 secretion was increased in the LDLr-/- mice. The composition of nascent VLDL was similar in both strains. To test whether the action of apoE depends on the presence of the LDLr, VLDL production was measured in LDLr-/- and apoE-/- LDLr-/- mice. Deletion of apoE on a LDLr-/- background still caused a 50% decrease of VLDL triglycerides and apoB production. The composition of nascent VLDL was again similar for both strains. We conclude that the effect of apoE on hepatic VLDL production is independent of the presence of the LDLr.


* This work was supported by Dutch Heart Foundation Grants NHS 96011 and 97067.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ To whom correspondence should be addressed: TNO Prevention and Health, Gaubius Laboratory, P. O. Box 2215, NL-2301 CE Leiden, The Netherlands. Tel.: 31-71-5181428; Fax: 31-71-5181904; E-mail: B.Teusink@pg.tno.nl.


Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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