Article Abstract:
It appears that a major gene with pleiotropic effects on LDL particle size and apolipoprotein B (apoB) levels may be the gene behind familial combined hyperlipidemia (FCH) in 40 studied families. The families were well-defined FCH families. FCH involves a common genetic mechanism that determines plasma apolipoprotein B levels and the dense LDL subfraction distribution. FCH is a common lipid disorder characterized by elevations of plasma cholesterol and/or triglyceride in first-degree relatives. A predominance of small, dense LDL particles and elevated apoB levels is found often in members of FCH families. A bivariate genetic analysis has been carried out to evaluate the hypothesis that there is a common genetic mechanism for elevation of apoB levels and predominance of small, dense LDL particles in FCH.
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Article Abstract:
A genetically based association of familial combined hyperlipidemia (FCH) and small, dense low density lipids (LDL) exists. Genetic determinants for LDL particle size are shared among FCH famlilies and the more general population at risk for coronary artery disease (CAD). Small, dense LDL particles have been associated consistently with premature CAD, hypertriglyceridemia, and FCH. Four candidate-gene loci have been seen to be linked with LDL particle size in a study of families more prone to CAD. Members of 18 families, having 481 members total, were typed for genetic markers at the four loci.
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Article Abstract:
Linkage of familial combined hyperlipidemia (FCHL), a common lipid familial lipid disorder, with a locus on chromosome 11 is discussed, as is the genome scan for it. It appears that FCHL, which is present in 10-20% of those with premature coronary heart disease, is complex and heterogeneous.
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