The present study reports on the interaction between basal
triglyceride and
high density lipoprotein (
HDL) cholesterol in determining the magnitude of postprandial triglyceridemia. The
vitamin A fat-loading test was used to label intestinally derived
triglyceride-rich particles after a high fat meal in 18 subjects with low
HDL cholesterol and 6 control subjects who had normal fasting
triglyceride and
HDL cholesterol levels. The patients with low
HDL cholesterol were divided into 2 groups on the basis of their basal
triglyceride concentrations; 11 had normal
triglyceride levels, and 7 had elevated serum
triglycerides (HTG). In the HTG-low HDL group, the incremental area under the
triglyceride curve was significantly greater (P less than 0.0003) than that in the other 2 groups, between whom no significant differences in
triglyceride response were observed.
Retinyl palmitate levels measured in whole plasma, an Sf greater than 1000
chylomicron fraction, and an Sf less than 1000 nonchylomicron fraction were also significantly greater in low HDL subjects with HTG, while the concentrations in low HDL subjects with normal
triglyceride levels and control subjects were similar. Although basal
HDL cholesterol levels in all study subjects were negatively correlated with the area under the incremental
triglyceride curve (r = -0.42; P less than 0.05), this correlation was weak, in contrast to the correlation between fasting
triglyceride levels and incremental
triglyceride area (r = 0.56; P less than 0.005). Furthermore, basal
HDL cholesterol levels did not correlate with the area under the
chylomicron or nonchylomicron curves, whereas basal
triglyceride levels were significantly correlated (P = 0.0001) with both of these variables. The HDL particles of both low HDL groups had a significantly higher proportion of
triglyceride compared to the HDL particles in the control subjects. In conclusion, 1) fasting
triglyceride levels are a more powerful
indicator of the postprandial
lipid response than basal
HDL cholesterol in subjects with low
HDL cholesterol levels; 2) patients with low
HDL cholesterol levels do not preferentially accumulate
chylomicron remnants after a meal unless they have coexisting
hypertriglyceridemia; and 3) abnormalities in the levels of
triglyceride-rich particles post-prandially are unlikely to be responsible for the increased incidence of
atherosclerosis in low HDL patients who are normotriglyceridemic.