Changes in the concentration and distribution of lipoprotein (a) in plasma after fat intake

To clarify the association between apo(a) and TG-rich lipoproteins, we studied changes in plasma Lp(a) concentration and apo(a) distribution in lipoprotein fractions after fat intake. The subjects were 15 hyperlipidemic patients and 3 healthy volunteers with fasting Lp(a) concentrations ranging from 2.5-52 mg/dl. They were given a fatty meal (50 g fat/m2 and 60 mg retinyl palmitate) after a 12-hour overnight fast and venous blood samples were taken at 0, 3, 4.5, 6, 7.5, 9, 12 and 24 hours. Fractions of sf > 400, sf 20-400 and d > 1.006 g/ml were isolated from plasma samples by ultracentrifugation. Plasma Lp(a) levels increased transiently at 4.5 hours, decreased between 4.5 and 12 hours, and recovered almost to initial levels by the next morning. Plasma Lp(a) peaked before the plasma RP peak appeared. Apo(a) associated with TG-rich lipoprotein fractions increased and apo(a) in the d > 1.006 fraction decreased after fat intake in most of the subjects, suggesting the transfer of apo(a) from the d > 1.006 fraction to the TG-rich lipoproteins. The increase in TG-rich lipoprotein apo(a) correlated with the RP area under the curve (r=0.79, p<0.05) and the decrease in d > 1.006 apo(a) (r = 0.80, p < 0.05). This distributional change of apo(a) after fat intake was confirmed by gel filtration and density gradient ultracentrifugation. Transfer of apo(a) from the main Lp(a) fraction of the plasma obtained from a subject with a high Lp(a)level to the TG-rich lipoprotein fraction of the plasma obtained 4.5 hours after fat intake from a subject with a low plasma Lp(a) level was also shown in vitro by density gradient ultracentrifugation. Our studies revealed a significant association between apo(a) and TG-rich lipoproteins in the postprandial. Further studies are necessary to clarify the pathophysiological role of Lp(a) in TG-rich lipoproteins.