Pleiotropy and Heterogeneity in the Expression of Atherogenic Lipoproteins: The IRAS Family StudyHokanson J.E.a · Langefeld C.D.b · Mitchell B.D.c · Lange L.A.b · Goff Jr. D.C.b · Haffner S.M.d · Saad M.F.e · Rotter J.I.e,f
aDepartment of Preventive Medicine and Biometrics, University of Colorado Health Sciences Center, Denver, Colo., bWake Forest University School of Medicine, Winston-Salem, N.C., cUniversity of Maryland, Baltimore, Md., dUniversity of Texas Health Sciences Center at San Antonio, San Antonio, Tex., eUniversity of California at Los Angeles, fCedars-Sinai Medical Center, Los Angeles, Calif., USA
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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 (ρg) and environmental (ρe) correlations between apoB, LDL-C, HDL-C, and triglyceride (Tg) from Hispanic and African American families of the IRAS Family Study. Results: Heritability estimates (hcirc;2) indicate significant genetic effects on apoB (hcirc;2 = 0.46 ± 0.05), LDL-C (hcirc;2 = 0.40 ± 0.05), HDL-C (hcirc;2 = 0.47 ± 0.05), and Tg (hcirc;2 = 0.35 ± 0.05) (all p < 0.001). Genetic and environmental correlations were strong for apoB – LDL-C (ρg = 0.87, ρe = 0.84), apoB – Tg (ρg = 0.38, ρe = 0.65), and HDL-C – Tg (ρg = –0.42, ρe = –0.46). Environmental correlations were strong for apoB – HDL-C (ρe = –0.40), LDL-C – HDL-C (ρe = –0.24), and Tg – LDL-C (ρe = 0.33) with weak genetic correlations for these pairs (ρg = –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.
© 2003 S. Karger AG, Basel
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