Atherosclerosis and Lipoproteins |
2
allele (24.76±0.08 vs 24.94±0.02 nm, P=0.02), and
this was evident for both E2/E3 (24.77±0.09 nm) and E2/E4 (24.69±0.08
nm) phenotypes. Although there was a negative relation between
LDL diameter and plasma triglyceride, the effect of apo E2
was still evident with adjustment for triglyceride. In
multiple regression analysis, the significant determinants of
LDL diameter were gender (with females having larger particles than
males), body mass index, and the presence (or absence) of E2. HDL
particle sizes and compositions were determined on fasting samples and,
additionally, 5 and 8 hours after a fat-rich meal for 48
coronary heart disease cases and 49 control subjects. Fasting
HDL particle sizes were not related to the presence of E2 but were
significantly smaller for subjects possessing an
4 allele
(8.09±0.08 vs 8.39±0.05 nm, P=0.003) and were
negatively related to plasma triglyceride. However, the
effect of E4 persisted after adjustment for triglyceride.
In a multiple regression analysis, the only significant
determinant of fasting HDL diameter was the presence (or absence) of E4
with fasting plasma triglyceride just failing to reach
significance (P=0.06). There was a postprandial increase
in HDL diameter that was less marked in subjects with coronary
heart disease. The postprandial increase in HDL diameter was of
sufficient magnitude to result in size reclassification of HDL
particles. The influence of E4 was also evident at both postprandial
time points. Compositional analysis demonstrated that the
increase in HDL diameters postprandially could be attributed to
triglyceride enrichment, with an accompanying fall in
cholesterol ester content. Phospholipid changes
postprandially were biphasic with an initial fall followed by a rise in
concentration. The increase in triglyceride content was
significantly less in those subjects with angina despite an equivalent
rise in plasma triglyceride. The present study
demonstrates significant, but different, effects of variation in apo E
phenotype on the particle sizes of both HDL and LDL. Such
effects were still evident with adjustment for differences in plasma
triglyceride and suggests that variation in apo E
phenotype exerts effects on lipoprotein particle sizes by
mechanisms additional to those dependent on change in plasma
triglyceride.
Key Words: apo E LDL particle size HDL particle size triglyceride coronary heart disease postprandial
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