In subjects with familial hypercholesterolemia, the rate of cholesteryl ester mass transfer to apolipoprotein B-containing lipoproteins is significantly enhanced, with triglyceride-rich, light LDL subspecies acting as preferential acceptors.
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May promote atherogenesis in heterozygous FH; leaves open causal role in events pending prospective data.
Guérin et al. (1994) studied this question.
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