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A more recent version of this article appeared on July 1, 2004

Papers In Press, published online ahead of print April 21, 2004
J. Lipid Res., doi:10.1194/jlr.M300350-JLR200
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Submitted on August 15, 2003
Revised on March 31, 2004
Accepted on April 5, 2004

Postprandial chylomicrons: Potent vehicles for transporting cholesterol from endogenous cholesterol-rich lipoproteins and cell membranes to the liver via LCAT and CETP

Byung-Hong Chung, Ping Liang, Steve Doran, B. H. Simon Cho, and Frank Franklin

Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294

Corresponding Author: bhchung{at}uab.edu; bhchung@netscape.com

We examined whether postprandial (PP) chylomicrons (CM) can serve as vehicles for transporting cholesterol from endogenous cholesterol-rich lipoprotein (CRL) fraction (LDL and HDL) and cell membranes to the liver via LCAT and CETP activities. During incubation of fresh fasting and PP plasma containing {3h}-cholesterylester (CE)-labeled CRL, both CM and VLDL served as acceptors of {3h}-CE or cholesterol from CRL. The presence of CM in PP plasma suppressed the ability of VLDL to accept {3H-CE} from CRL. In reconstituted plasma containing an equivalent amount of triglycerides (TG) from isolated fasting VLDL or PP CM, VLDL was somewhat (1.3-1.5x) more potent than CM in accepting cholesterol or {3h}-CE from CRL. However, because a CM particle contains much (40x) more TG molecules than a VLDL particle, CM is in effect about 31x more potent than VLDL. When incubated with RBC as a source for cell membrane cholesterol, the cholesterol content of all lipoproteins in either fasting or PP plasma increased via acceptance of cholesterol from RBC. In PP plasma, the increase in cholesterol content of CM (485%) was much greater than that of VLDL (74%), LDL (13%) and HDL (30%). The increase in cholesterol content of LDL (20%) and HDL (37%) in fasting plasma was significantly greater than that in PP plasma, suggesting that the presence of CM in plasma suppressed the ability of endogenous lipoproteins to accept cholesterol from RBC. Our data suggests that PP CM may play an important role in promoting reverse cholesterol transport (RCT) in vivo by serving as the potent ultimate vehicle for transport to the liver of cholesterol released from cell membranes into plasma via LCAT and CETP


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