title: Apolipoprotein E polymorphism modulates the association between obesity and dyslipidemias during young adulthood: The Bogalusa Heart Study.
abstract: To elucidate to what extent apolipoprotein (apo) E polymorphism modulates obesity-induced dyslipidemias during young adulthood, longitudinal data on 759 individuals (72% white/28% black; initial and follow-up mean age, 25.9 and 32.7 years) were examined. Among both races and the total sample, the apo E2 group (with E2/2 or E2/3 phenotype) had significantly lower and the apo E4 (with E4/4 or E3/4 phenotype) group higher low-density lipoprotein (LDL) cholesterol than the apo E3 (with E3/3 phenotype) group at both examinations. In addition, the apo E2 group displayed higher high-density lipoprotein (HDL) cholesterol in the total sample. No allele-specific effect was noted for the longitudinal changes (Delta). An increase in Delta adiposity, measured as Delta body mass index (BMI), was accompanied by higher increase in Delta LDL cholesterol in the e4 carriers than the e2 carriers among the whites (P <.05) and the total sample (P <.01); an increase in Delta triglycerides and decrease in Delta HDL cholesterol in the e2 carriers than the e4 carriers among all the groups (P <.05 to.001). Among the apo E phenotype groups, the incidence of high (>75th percentile specific for race and sex) LDL cholesterol at follow-up was in the order E4 > E3 > E2 both in the obese (BMI > 30; P for trend =.033) and the nonobese (BMI < 25; P for trend =.035) groups. Although the increase of low (<25th percentile specific for race and sex) HDL cholesterol or high triglycerides showed no apo E phenotype-specific trend, the incidence of high triglycerides without high LDL cholesterol was in the order E2 > E3 > E4 only in the obese group (P for trend =.025). The prevalence trend for dyslipidemias at follow-up among the persistently obese and nonobese groups also gave similar results. Thus, apo E gene locus influences not only the levels of certain lipoprotein variables during young adulthood, but also modulates the association between obesity and dyslipidemias.
authors.affiliation: Tulane Center for Cardiovascular Health, New Orleans, LA 70112, USA.
authors.forename: S R
authors.initials: SR
authors.lastname: Srinivasan
authors.forename: C
authors.initials: C
authors.lastname: Ehnholm
authors.forename: A
authors.initials: A
authors.lastname: Elkasabany
authors.forename: G S
authors.initials: GS
authors.lastname: Berenson
mesh_terms: D000328:Adult; D000483:Alleles; D001057:Apolipoproteins E / Q000235:genetics*; D015992:Body Mass Index; D002318:Cardiovascular Diseases / Q000209:etiology; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015331:Cohort Studies; D005500:Follow-Up Studies; D006801:Humans; D006949:Hyperlipidemias / Q000150:complications / Q000453:epidemiology / Q000235:genetics*; D008145:Louisiana / Q000453:epidemiology; D009765:Obesity / Q000097:blood / Q000150:complications / Q000235:genetics*; D010641:Phenotype; D015995:Prevalence; D044469:Racial Groups; D014280:Triglycerides / Q000097:blood
chemical_list: D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides