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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:2759-2764.)
© 1997 American Heart Association, Inc.

Articles

The Role of a Triplet Repeat Sequence of the Very Low Density Lipoprotein Receptor Gene in Plasma Lipid and Lipoprotein Level Variability in Humans

Nicole Helbecque; Jean Dallongeville; Valérie Codron; Dominique Arveiler; Jean-Bernard Ruidavets; Alun Evans; François Cambien; Jean-Charles Fruchart; ; Philippe Amouyel

From the Service d'Epidémiologie et de Santé Publique—INSERM CJF 95-05, Institut Pasteur de Lille (N.H., V.C., P.A.); INSERM U 325, Institut Pasteur de Lille (J.D., J.-C.F.), Lille France; Laboratoire d'Epidémiologie et de Santé Publique, Strasbourg France (D.A.); Département d'Epidémiologie, Faculté de Médecine, Toulouse (J.-B.R.) France; Department of Epidemiology and Public Health, The Queen's University of Belfast, Belfast, Northern Ireland (A.E.); INSERM SC7, Paris, France (F.C.)

Correspondence to Pr Philippe Amouyel, Service d'Epidémiologie et de Santé Publique et INSERM, CJF 95-05, Institut Pasteur de Lille, 1 rue du Professeur Calmette, 59019 Lille Cedex, France.

Abstract The biological role of the very low density lipoprotein receptor (VLDL-R) in humans is not yet elucidated. This cellular receptor binds apolipoprotein E (apoE)-containing lipoparticles and is mainly expressed in peripheral tissues. The VLDL-R gene contains a polymorphic triplet (CGG) repeat located 19 bp upstream of the initiation codon. We explored the allelic distribution of this repeat in 1384 subjects of European Caucasian origin, 609 of them surviving a myocardial infarction. Six alleles corresponding to 5, 6, 7, 8, 9, and 11 repeats were detected in this population. The alleles 5, 8, and 9 were the most frequent, with frequencies of 0.413, 0.275, and 0.292, respectively. No association was found between the VLDL-R polymorphism and myocardial infarction. In controls without lipid lowering treatment, a statistically significant interaction between VLDL-R genotype and apoE phenotype was found for plasma triglycerides (P<.04), suggesting a gene-gene interaction. There was also a main effect of the VLDL-R polymorphism on LpE:B and LpA-I. The VLDL-R 9 allele was associated with lower levels of plasma LpE:B (P<.05) and higher concentrations of plasma LpA-I (P<.01) than the other alleles. These results suggest that VLDL-R has a modest influence on circulating lipoproteins in humans.

Key Words: VLDL receptor • triglyceride-rich lipoproteins • polymorphism • lipoprotein metabolism