To quantify the effect of the apolipoprotein (apo) E polymorphism on the magnitude of postprandial lipemia,
we have defined its role in determining the response to a single high-fat meal in a large sample of (N = 474)
individuals taking part in the biethnic Atherosclerosis Risk in Communities Study. The profile of postprandial
response in plasma was monitored over 8 h by triglyceride, triglyceride-rich lipoprotein (TGRL)-triglyceride,
apo B-48/apo B-100 ratio, and retinyl palmitate concentrations, and the apo E polymorphism was determined
by DNA amplification and digestion. The frequency of the apo E alleles and their effects on fasting lipid levels
in this sample were similar to those reported elsewhere. Postprandial plasma retinyl palmitate response to a
high-fat meal with vitamin A was significantly different among apo E genotypes, with delayed clearance in
individuals with an £2 allele, compared with £3/3 and £3/4 individuals. In the sample of 397 Caucasians,
average retinyl palmitate response was 1,489 ttg/dl in £2/3 individuals, compared with 1,037 jig/dl in £3/3
individuals and 1,108 Ftg/dl in £3/4 individuals. The apo E polymorphism accounted for 7.1% of the
interindividual variation in postprandial retinyl palmitate response, a contribution proportionally greater than
its well-known effect on fasting LDL-cholesterol. However, despite this effect on postprandial retinyl palmitate,
the profile of postprandial triglyceride response was not significantly different among apo E genotypes. The
profile of postprandial response was consistent between the sample of Caucasians and a smaller sample of black
subjects. While these data indicate that the removal of remnant particles from circulation is delayed in subjects
with the £2/3 genotype, there is no reported evidence that the £2 allele predisposes to coronary artery disease
(CAD). The results of this study provide not only a reliable estimate of the magnitude of the effect of the apo
E polymorphism on various measurements commonly used to characterize postprandial lipemia, but also provide
mechanistic insight into the effects of the apo E gene polymorphism on postprandial lipemia and CAD
