Heritability of LDL peak particle diameter in the Quebec family study

被引:19
作者
Bossé, Y
Vohl, MC
Després, JP
Lamarche, B
Rice, T
Rao, DC
Bouchard, C
Pérusse, L [1 ]
机构
[1] Univ Laval, Phys Act Sci Lab, Div Kinesiol, Dept Social & Prevent Med, Quebec City, PQ G1K 7P4, Canada
[2] Univ Laval, CHUL, Res Ctr, Lipid Res Ctr, Quebec City, PQ, Canada
[3] Univ Laval, Dept Food Sci & Nutr, Quebec City, PQ, Canada
[4] Univ Laval, Inst Nutraceut & Funct Food, Quebec City, PQ, Canada
[5] Quebec Heart Inst, Quebec City, PQ, Canada
[6] Washington Univ, Sch Med, Div Biostat, St Louis, MO USA
[7] Pennington Biomed Res Ctr, Baton Rouge, LA USA
关键词
genetics; lipoproteins; LDL size;
D O I
10.1002/gepi.10272
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
LDL size has been associated with the risk of coronary heart disease. The objective of the present study was to verify whether familial factors influence LDL peak particle diameter (LDL-PPD), a quantitative trait reflecting the size of the major LDL subclass. LDL-PPD was measured by 2-16% polyacrylamide gradient gel electrophoresis in 681 members of 236 nuclear families participating in the Quebec Family Study. LDL-PPD was adjusted for age (LDL-PPD1), age and body mass index (LDL-PPD2), or age, body mass index, and plasma triglyceride levels (LDL-PPD3) separately in men and women. The residual scores were used to test for familial aggregation, using an ANOVA and to compute maximum likelihood estimates of familial correlations. The ANOVA test revealed that family lines accounted for 47.4%, 46.7%, and 48.9% of the variance in the LDL-PPD1, LDL-PPD2, and LDL-PPD3 phenotypes, respectively. The pattern of familial correlations revealed no significant spouse correlations but significant parent-offspring and sibling correlations for the three LDL-PPD phenotypes, with maximal heritability estimates of 59%, 58%, and 52% for LDL-PPD1, LDL-PPD2, and LDL-PPD3, respectively. These results suggest that LDL-PPD strongly aggregates in families, and that the familial resemblance appears to be primarily attributable to genetic factors. Genes responsible for this genetic contribution remain to be identified. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:375 / 381
页数:7
相关论文
共 24 条
[1]   NEW LOOK AT STATISTICAL-MODEL IDENTIFICATION [J].
AKAIKE, H .
IEEE TRANSACTIONS ON AUTOMATIC CONTROL, 1974, AC19 (06) :716-723
[2]   GENETICS OF LDL SUBCLASS PHENOTYPES IN WOMEN TWINS - CONCORDANCE, HERITABILITY, AND COMMINGLING ANALYSIS [J].
AUSTIN, MA ;
NEWMAN, B ;
SELBY, JV ;
EDWARDS, K ;
MAYER, EJ ;
KRAUSS, RM .
ARTERIOSCLEROSIS AND THROMBOSIS, 1993, 13 (05) :687-695
[3]  
AUSTIN MA, 1988, AM J HUM GENET, V43, P838
[4]   INHERITANCE OF LOW-DENSITY-LIPOPROTEIN SUBCLASS PATTERNS IN FAMILIAL COMBINED HYPERLIPIDEMIA [J].
AUSTIN, MA ;
BRUNZELL, JD ;
FITCH, WL ;
KRAUSS, RM .
ARTERIOSCLEROSIS, 1990, 10 (04) :520-530
[5]   COMPLEX SEGREGATION ANALYSIS OF LDL PEAK PARTICLE DIAMETER [J].
AUSTIN, MA ;
JARVIK, GP ;
HOKANSON, JE ;
EDWARDS, K .
GENETIC EPIDEMIOLOGY, 1993, 10 (06) :599-604
[6]  
Austin Melissa A., 1994, Current Opinion in Lipidology, V5, P395, DOI 10.1097/00041433-199412000-00002
[7]  
Bouchard C, 1996, PENN CTR N, V5, P470
[8]  
Bredie SJH, 1996, AM J HUM GENET, V58, P812
[9]  
Comuzzie AG, 1997, GENET EPIDEMIOL, V14, P975, DOI 10.1002/(SICI)1098-2272(1997)14:6<975::AID-GEPI69>3.0.CO
[10]  
2-I