title: Pleiotropy and heterogeneity in the expression of atherogenic lipoproteins: the IRAS Family Study.
abstract: OBJECTIVE
  Dyslipidemia is an important determinant of coronary disease. Phenotypic correlations between atherogenic lipids are well established, but the contribution of common genetic influences is less clear.
  
  
  METHODS
  This study investigates the pair-wise genetic (rhog) and environmental (rhoe) correlations between apoB, LDL-C, HDL-C, and triglyceride (Tg) from Hispanic and African American families of the IRAS Family Study.
  
  
  RESULTS
  Heritability estimates (ĥ2) indicate significant genetic effects on apoB (ĥ2=0.46+/-0.05), LDL-C (ĥ2=0.40+/-0.05), HDL-C (ĥ2=0.47+/-0.05), and Tg (ĥ2=0.35+/-0.05) (all p<0.001). Genetic and environmental correlations were strong for apoB-LDL-C (rhog=0.87, rhoe=0.84), apoB-Tg (rhog=0.38, rhoe=0.65), and HDL-C-Tg (rhog=-0.42, rhoe=-0.46). Environmental correlations were strong for apoB-HDL-C (rhoe=-0.40), LDL-C-HDL-C (rhoe=-0.24), and Tg-LDL-C (rhoe=0.33) with weak genetic correlations for these pairs (rhog=-0.09, 0.10, 0.09 respectively).
  
  
  CONCLUSIONS
  These results suggest multiple pathways leading to atherogenic dyslipidemia. There are common genetic and environmental influences contributing to variations in apoB and LDL-C as well as apoB and Tg. In addition, the inverse relation between Tg and HDL-C appears to have both genetic and environmental basis. Identifying genes involved in atherogenic dyslipidemia will require careful dissection of the genetic architecture of these pathways.
authors.affiliation: Department of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, Colo. 80262, USA. john.hokanson@uchsc.edu
authors.forename: John E
authors.initials: JE
authors.lastname: Hokanson
authors.forename: Carl D
authors.initials: CD
authors.lastname: Langefeld
authors.forename: Braxton D
authors.initials: BD
authors.lastname: Mitchell
authors.forename: Leslie A
authors.initials: LA
authors.lastname: Lange
authors.forename: David C
authors.initials: DC
authors.lastname: Goff
authors.forename: Steven M
authors.initials: SM
authors.lastname: Haffner
authors.forename: Mohammad F
authors.initials: MF
authors.lastname: Saad
authors.forename: Jerome I
authors.initials: JI
authors.lastname: Rotter
mesh_terms: D000328:Adult; D001741:Black or African American / Q000235:genetics; D001055:Apolipoproteins B / Q000235:genetics*; D008076:Cholesterol, HDL / Q000235:genetics*; D008078:Cholesterol, LDL / Q000235:genetics*; D004198:Disease Susceptibility; D005192:Family Health; D005260:Female; D018740:Genetic Heterogeneity; D006630:Hispanic or Latino / Q000235:genetics; D006801:Humans; D006949:Hyperlipidemias / Q000235:genetics*; D008297:Male; D010641:Phenotype; D012307:Risk Factors; D014280:Triglycerides / Q000235:genetics*
chemical_list: D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides