The inherited low-density lipoprotein phenotype B is associated with an atherogenic profile of increased triglycerides and apolipoprotein B, and decreased HDL cholesterol.
The genetic locus responsible for small, dense LDL particles (phenotype B) is associated with a broader atherogenic lipid profile, highlighting its potential as a genetic marker for coronary heart disease risk.
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In a community-based study of 301 subjects from 61 nuclear families, two distinct phenotypes (denoted A and B) were identified by nondenaturing gradient gel electrophoretic analysis of low density lipoprotein (LDL) subclasses. Phenotype A was characterized by predominance of large, buoyant LDL particles, and phenotype B consisted of a major peak of small, dense LDL particles. Previous analysis of the family data by complex segregation analysis demonstrated that these phenotypes appear to be inherited as a single-gene trait. In the present study, the phenotypes were found to be closely associated with variations in plasma levels of other lipid, lipoprotein, and apolipoprotein measurements. Specifically, phenotype B was associated with increases in plasma levels of triglyceride and apolipoprotein B, with mass of very low and intermediate density lipoproteins, and with decreases in high density lipoprotein (HDL) cholesterol, HDL2 mass, and plasma levels of apolipoprotein A-I. Thus, the proposed genetic locus responsible for LDL subclass phenotypes also results in an atherogenic lipoprotein phenotype.
Austin et al. (Wed,) reported a other. The inherited low-density lipoprotein phenotype B is associated with an atherogenic profile of increased triglycerides and apolipoprotein B, and decreased HDL cholesterol.