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J Lipid Res. 1988 Jul;29(7):925-36.

Plasma apolipoprotein changes in the triglyceride-rich lipoprotein fraction of human subjects fed a fat-rich meal.

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Lipid Metabolism Laboratory, USDA Human Nutrition Research Center on Aging, Tufts University, Boston, MA 02111.


Twenty two subjects (9 males, 13 females) were fed a fat-rich meal (1 g of fat/kg body weight). Triglyceride-rich lipoproteins (TRL) were isolated by ultracentrifugation (d less than 1.006 g/ml) from blood drawn 0, 3, 6, 9, and 12 hr after the meal. Plasma triglyceride increased then decreased postprandially, while plasma apoA-I and apoB concentrations decreased. TRL triglyceride, TRL total protein, and TRL apoB concentrations all increased then decreased after the fat-rich meal. Postprandial rise in plasma triglyceride was significantly correlated with fasting plasma triglyceride levels (r = 0.66, P less than 0.001); postprandial rise in TRL triglyceride was significantly correlated with fasting TRL triglyceride levels (r = 0.58, P less than 0.01); postprandial rise in TRL apoB was not, however, significantly correlated with fasting TRL apoB levels (r = 0.37, N.S.). TRL apolipoproteins were separated by polyacrylamide gradient (4-22.5%) gel electrophoresis and protein bands were scanned in two dimensions with a laser densitometer. Relative postprandial changes in the concentration of the TRL apolipoproteins were determined. TRL apoB-100, apoB-48, apoE, and apoC increased then decreased postprandially. The increase in TRL apoB-100 after the fat-rich meal was confirmed in 8 subjects by direct measurement of apoB-100 with a monoclonal antibody ELISA assay. ApoA-I concentration in TRL was unchanged. Albumin in the TRL fraction was significantly increased 12 hr after the meal. Subjects with a greater magnitude of postprandial triglyceridemia had a greater increase in TRL triglyceride and TRL apoB, but their TRL apoB-100/apoB-48 ratios were not different from subjects with less pronounced triglyceridemia. Assuming that plasma TRL containing apoB-100 are predominantly derived from the liver, our data suggest that triglyceride-rich lipoproteins from both the liver and intestine make a significant contribution to postprandial triglyceridemia.

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