Flow B L, Mott G E, Kelley J L
Atherosclerosis. 1982 May;43(1):83-94. doi: 10.1016/0021-9150(82)90101-0.
Genetic effects on serum lipoprotein and apoprotein concentrations were investigated using a paternal half-sib design with 79 progeny of 6 sires. Significant differences (P less than 0.05) were observed among sire progeny groups at 4-6 years of age for serum cholesterol, HDL cholesterol and apoA-I concentrations. A sire effect (P less than 0.10) also was observed for VLDL + LDL cholesterol concentrations, but differences were not observed (P greater than 0.10) among sire progeny groups for apoB concentrations. Estimates of heritability were 0.54 for serum cholesterol, 0.32 for VLDL + LDL cholesterol, 0.78 for HDL cholesterol, 0.56 for apoA-I, and 0.20 for apoB concentration. Genetic (rg) and environmental (re) correlations among serum cholesterol, lipoprotein cholesterol, and apoprotein concentrations were positive except for the negative genetic relationships of apoA-I with apoB (rg = -0.74) and with VLDL + LDL cholesterol (rg = -0.30) concentrations. The phenotypic correlation (rp = 0.31) of VLDL + LDL cholesterol with HDL cholesterol was due entirely to the genetic contribution (0.31) since the environmental contribution was zero. The positive genetic relationship (rg = 0.62) of VLDL + LDL cholesterol and HDL cholesterol may be due to biochemical mechanisms controlling cholesterol turnover since the genetic correlations of VLDL + LDL cholesterol and HDL cholesterol with cholesterol turnover rate were both negative (-0.43 and -0.68, respectively). A strong negative genetic correlation (rg = -0.95) was observed between apoA-I and cholesterol turnover, a finding that suggests a close physiologic relationship between these variables.