title: Influence of cholesteryl ester transfer protein, peroxisome proliferator-activated receptor alpha, apolipoprotein E, and apolipoprotein A-I polymorphisms on high-density lipoprotein cholesterol, apolipoprotein A-I, lipoprotein A-I, and lipoprotein A-I:A-II concentrations: the Prospective Epidemiological Study of Myocardial Infarction study.
abstract: The plasma level of high-density lipoprotein cholesterol (HDL-C) is known to be inversely associated with cardiovascular risk. However, besides lifestyle, gene polymorphism may influence the HDL-C concentration. The aim of this study was to investigate the possibility of interactions between CETP, PPARA, APOE, and APOAI polymorphisms and HDL-C, apolipoprotein (apo) A-I, lipoprotein (Lp) A-I, and Lp A-I:A-II in a sample selected from the Prospective Epidemiological Study of Myocardial Infarction (PRIME) study population who remained free of cardiovascular events over 5 years of follow-up. Healthy individuals (857) were randomly selected for genotyping the PRIME study subjects. The population was selected so as to provide 25% of subjects in the lowest tertile of HDL-C (< or = 28 mg/dL) in the whole PRIME study sample, 25% of subjects in the highest tertile of HDL-C (> or = 73 mg/dL), and 50% of subjects in the medium tertile of HDL-C (28-73 mg/dL). Genotyping was performed by using a polymerase chain reaction system with predeveloped TaqMan allelic discrimination assay. The CETP A373P rare allele c was less frequent in the group of subjects with high HDL-C, apo A-I, Lp A-I, and Lp A-I:A-II concentrations. Apolipoprotein A-I and Lp A-I were also found to be higher in the presence of the epsilon2 allele coding for APOE. The effect of the CETP A373P rare allele c on HDL-C was independent of all tested parameters except triglycerides. The respective effect of these polymorphisms and triglycerides on cardiovascular risk should be evaluated prospectively.
authors.affiliation: Faculté de Pharmacie, Université de Nantes, Laboratoire de Biochimie, EA3823, 1 rue Gaston Veil, 44035 Nantes, France.
authors.forename: Hong Quang
authors.initials: HQ
authors.lastname: Do
authors.forename: Hassan
authors.initials: H
authors.lastname: Nazih
authors.forename: Gérald
authors.initials: G
authors.lastname: Luc
authors.forename: Dominique
authors.initials: D
authors.lastname: Arveiler
authors.forename: Jean
authors.initials: J
authors.lastname: Ferrières
authors.forename: Alun
authors.initials: A
authors.lastname: Evans
authors.forename: Philippe
authors.initials: P
authors.lastname: Amouyel
authors.forename: François
authors.initials: F
authors.lastname: Cambien
authors.forename: Pierre
authors.initials: P
authors.lastname: Ducimetière
authors.forename: Jean-Marie
authors.initials: JM
authors.lastname: Bard
mesh_terms: D016632:Apolipoprotein A-I / Q000097:blood / Q000235:genetics*; D016633:Apolipoprotein A-II / Q000097:blood*; D001057:Apolipoproteins E / Q000235:genetics*; D053480:Cholesterol Ester Transfer Proteins / Q000235:genetics*; D008076:Cholesterol, HDL / Q000097:blood*; D015331:Cohort Studies; D004247:DNA / Q000097:blood / Q000235:genetics; D005602:France; D005838:Genotype; D006801:Humans; D008019:Life Style; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000453:epidemiology* / Q000235:genetics*; D009660:Northern Ireland; D047493:PPAR alpha / Q000235:genetics*; D011110:Polymorphism, Genetic
chemical_list: D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D001057:Apolipoproteins E; D053480:Cholesterol Ester Transfer Proteins; D008076:Cholesterol, HDL; D047493:PPAR alpha; D004247:DNA