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Volume 271, Number 37, Issue of September 13, 1996 pp. 22422-22427
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Role of the Low Density Lipoprotein (LDL) Receptor Pathway in the Metabolism of Chylomicron Remnants
A QUANTITATIVE STUDY IN KNOCKOUT MICE LACKING THE LDL RECEPTOR, APOLIPOPROTEIN E, OR BOTH

(Received for publication, October 16, 1995, and in revised form, March 27, 1996)

From the Third Department of Internal Medicine, Faculty of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan

Two receptor pathways are thought to mediate the hepatic clearance of chylomicron remnants, (i) the low density lipoprotein receptor (LDLR) pathway and (ii) non-LDLR pathway. The current study was undertaken to quantitatively assess the contribution of each receptor pathway to hepatic catabolism of chylomicron remnants, by using mice that are deficient in apolipoprotein E (apoE) (apoE(/)), the LDLR (LDLR(/)), and both (apoE(/);LDLR(/)). Vitamin A fat tolerance tests showed that the area under the curves of the plasma excursions of retinyl ester in the LDLR(/), apoE(/), and apoE(/);LDLR(/) mice were 4, 12, and 12 times larger than those in wild-type mice. The retinyl ester accumulated in the plasma of the LDLR(/) mice was distributed in larger subfractions of triglyceride-rich lipoproteins, chylomicrons through very low density lipoprotein-C. These results indicate that the LDLR constitutes the major pathway for the clearance of retinyl ester. In support of this, agarose gel electrophoresis revealed that an oral fat load resulted in retention of chylomicrons in the LDLR(/) mice, which was not seen in wild-type mice. The observation that the apoE(/) mice showed larger retinyl ester excursion than LDLR(/) mice indicates that an apoE-dependent non-LDLR pathway is involved in the rest of the clearance of the retinyl ester. Together, we conclude that the LDLR pathway plays a significant role in the chylomicron remnant metabolism in mice fed a normal chow.

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