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Journal of Lipid Research, Vol. 43, 1652-1660, October 2002
Copyright © 2002 by Lipid Research, Inc.

Cholesteryl ester flux from HDL to VLDL-1 is preferentially enhanced in type IIB hyperlipidemia in the postprandial state

Maryse Guerin^1,*, Pascal Egger^*, Céline Soudant^*, Wilfried Le Goff^*, Arie van Tol, Reynald Dupuis and M. John Chapman^*

^* Institut National de la Santé et de la Recherche Médicale, INSERM Unité 551, Dyslipoproteinemia and Atherosclerosis, Hôpital de la Pitié, 75651 Paris, France
Department of Biochemistry, Erasmus University, Rotterdam, The Netherlands
Pfizer, Paris, France

¹ To whom correspondence should be addressed. e-mail: mguerin{at}infobiogen.fr

Postprandial triglyceride-rich lipoproteins (TRL) exert proatherogenic effects at the arterial wall, including lipid deposition. Following consumption of a mixed meal (1,200 kcal), plasma-mediated cellular free cholesterol (FC) efflux, lecithin:cholesterol acyltransferase (LCAT), and cholesteryl ester transfer protein (CETP) activities were determined in subjects (n = 12) displaying type IIB hyperlipidemia and compared with those in a normolipidemic control group (n = 14). The relative capacity of plasma to induce FC efflux from Fu5AH cells via the SR-BI receptor was significantly increased 4 h postprandially (+23%; P < 0.005) in the type IIB group, whereas it remained unchanged for postprandial plasma from normolipidemic subjects. LCAT activity was significantly elevated 2 h postprandially in both the IIB and control groups, (+46% and +36%, respectively; P < 0.005 vs. respective baseline value). In type IIB subjects, total cholesteryl ester (CE) mass transfer from HDL to total TRL [chylomicrons (CMs) + VLDL-1 + VLDL-2 + IDL] increased progressively from 15 ± 2 µg CE/h/ml at baseline to 28 ± 2 µg CE transferred/h/ml (+87%; P = 0.0004) at 4 h postprandially. CE transfer to CMs and VLDL-1 was preferentially stimulated (2.6-fold and 2.3-fold respectively) at 4 h in IIB subjects and occurred concomitantly with elevation in mass and particle number of both CMs (2.3-fold) and VLDL-1 (1.3-fold). Furthermore, in type IIB subjects, CETP-mediated total CE flux over the 8 h postprandial period from HDL to potentially atherogenic TRL was significantly enhanced, and notably to VLDL-1 (32-fold elevation; P < 0.005), relative to control subjects. Such CE transfer flux was reflected in a significant postprandial increase in CE-TG ratio in both CMs and VLDL-1 in type IIB plasmas.

In conclusion, HDL-CE is preferentially targeted to VLDL-1 via the action of CETP during alimentary lipemia, thereby favoring formation and accumulation of atherogenic CE-rich remnant particles.

Abbreviations: CE, cholesteryl ester; CETP, cholesteryl ester transfer protein; TG, triglyceride; TRL, triglyceride-rich lipoprotein; CM, chylomicron; RCT, reverse cholesterol transport

Supplementary key words cholesteryl ester transfer protein • atherosclerosis • lecithin:cholesterol acyltransferase • cellular cholesterol efflux

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