Postprandial Lipoprotein Metabolism in Normal and Obese Subjects: Comparison after the Vitamin A Fat-Loading Test*

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Abstract
Abnormalities in fasting lipid and lipoprotein levels are known to occur in obesity and other hyperinsulinemic states. However, postprandial lipoprotein metabolism has not been studied systmatically in obese subjects using sensitive techniques to distinguish between triglyceride-rich liporportein particles derived from the intestine and the liver. In the present study the vitamin A fat-laoding test was used to label intestinally derived triglyceride-rich lipoprotein particles in the postprandial state. Lipid parameters in seven normolipidemic obese subjects [body mass index, 43.7 .+-. 2.81 kg/m2 (mean .+-. SEM)] were compared to those in eight matched normal weight controls (body mass index, 23.6 .+-. 0.72 kg/m2) during the 24-h period following ingestion of mixed meal with a high fat content to which vitamin A had been added. Although subjects were selected for normal fasting lipid levels, in the obese group fasting triglycerides were significantly higher (1.35 .+-. 0.12 v. 0.68 .+-. 0.08 mmol/L; P < 0.0005) and high density lipoprotein (HDL) cholesterol was lower (0.94 .+-. 0.08 vs. 1.35 .+-. 0.11 mmol/L; P < 0.01). The obese subjects had a greater postprandial triglyceride response to thet est meal (P < 0.05). The cumulative increment in total plasma triglycerides was 3.35-fold greater in obese than control subjects, while that of retinyl ester was only 1.63-fold greater, suggesting that a significant portion of the postprandial triglyceride response is due to endogenous hepatic lipoproteins. Postprandial plasma triglyceride and retinyl ester increment correlated with basal triglycerides (r = 0.72; P < 0.005 and r = 0.57; P < 0.03, respectively) and negatively with fasting HDL (r = -0.51; P < 0.05 and r = -0.60; P < 0.02, respectively). In the obese the HDL triglyceride content increased maximally 4 h postprandially (4.1% to 6.1%; P < 0.005) and phospholipid at 12 h (25.8% to 28.7%; P < 0.05), with lower cholesteryl ester (21.1% to 17.5%; P < 0.002) at 8 h, reflecting exchange of surface and core lipids with triglyceride-rich particles after the meal. In obese and control subjects the magnitude of HDL triglyceride enrichment after the meal correlated positively with the postprandial triglyceride increment (r = 0.74; P < 0.007) and negatively with the fasting HDL cholesterol concentration (r = -0.80; P = 0.002). We conclude that even normolipidemic obese subjects have greater postprandial lipemia and triglyceride enrichment of HDL after ingestion of a high fat meal. These data extend to the postprandial state the previously described observation that hyperinsulinemic obese subjects have abnormalities in basal lipid parameters which are potentially atherogenic.