title: Effect of apo E phenotype on plasma postprandial triglyceride levels in young male adults with and without a familial history of myocardial infarction: the EARS II study. European Atherosclerosis Research Study.
abstract: The goal of the present study was to assess whether the effect of the apolipoprotein E polymorphism on postprandial lipemia explained part of the risk attributable to familial history of coronary heart disease. Cases (n = 407) were students, aged between 18 and 28 years, whose fathers had a proven myocardial infarction before the age of 55 years. Age-matched controls (n = 415) were recruited from the corresponding student registers. Blood was obtained after an overnight fast and at 2, 3, 4 and 6 h after ingestion of a fatty meal for triglyceride measurements. Apolipoprotein E phenotype was associated with postprandial triglyceride variability in both cases and controls. However, the apolipoprotein E-dependent triglyceride response was not significantly heterogeneous between cases and controls. In the pooled data, postprandial triglyceride levels were higher in carriers of the E2 and, to a lesser extent, of the E4 isoform, than in E3/3 homozygotes, independently of fasting triglyceride levels. At 6 h, triglyceride levels were increased by 21.2% (P < 0.01) in E2 carriers and 11.5% (P = 0.053) in E4 carriers by comparison to E3/3 subjects. These effects were not significantly different between regions. In conclusion, the effects of the apolipoprotein E polymorphism on postprandial triglyceridemia are similar across regions of Europe, and homogeneous in healthy young subjects with and without a family history of early myocardial infarction. This suggests that the influence of apolipoprotein E on myocardial infarction risk may be acting through mechanisms other than through effects on postprandial triglyceridemia.
authors.affiliation: Département d'athérosclérose and INSERM U-508, Institut Pasteur, Lille, France.
authors.forename: J
authors.initials: J
authors.lastname: Dallongeville
authors.forename: L
authors.initials: L
authors.lastname: Tiret
authors.forename: S
authors.initials: S
authors.lastname: Visvikis
authors.forename: D S
authors.initials: DS
authors.lastname: O'Reilly
authors.forename: M
authors.initials: M
authors.lastname: Saava
authors.forename: G
authors.initials: G
authors.lastname: Tsitouris
authors.forename: M
authors.initials: M
authors.lastname: Rosseneu
authors.forename: G
authors.initials: G
authors.lastname: DeBacker
authors.forename: S E
authors.initials: SE
authors.lastname: Humphries
authors.forename: U
authors.initials: U
authors.lastname: Beisiegel
mesh_terms: D000293:Adolescent; D000328:Adult; D000483:Alleles; D001057:Apolipoproteins E / Q000097:blood / Q000235:genetics*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D004041:Dietary Fats / Q000008:administration & dosage; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000235:genetics; D010641:Phenotype; D011110:Polymorphism, Genetic; D019518:Postprandial Period / Q000502:physiology*; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood*
chemical_list: D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004041:Dietary Fats; D014280:Triglycerides