Changes in the plasma lipoprotein distribution of apolipoproteins C-II, C-III1, C-III2 and apolipoprotein B after heparin-induced lipolysis.

The group of C apolipoproteins are involved in the catabolism of triacylglycerol-rich lipoproteins, C-II activating triacyglycerol lipolysis and C-III possibly preventing premature removal of the particle. In normal subjects, C-II, C-III1 and C-III2 exchange between very low density (VLDL) and high density lipoprotein (HDL) at similar rates and catabolism appears to occur with HDL. In the present studies in one normal and in four subjects with moderate-to-severe hypertriglyceridemia, the metabolism of the C apolipoproteins was studied before and during maximal lipolysis induced with heparin. Radioiodinated triacylglycerol-rich lipoproteins were injected and the specific activity-time curves for C-II, C-III1, C-III2 and B proteins were analyzed in triacylglycerol-rich lipoproteins and HDL. Heparin infusion caused rapid and proportional transfer of each C apolipoprotein from triacylglycerol-rich lipoproteins to HDL. In the two most hyperlipemic men, a substantial fraction (over 90%) of apolipoprotein C mass lost from triacylglycerol-rich lipoproteins was not recoverable in HDL, whereas in the normal subject this was less than 15% and intermediate in the other two hypertriglyceridemic men. This indicates a new potential catabolic pathway for C apolipoproteins, direct loss from the circulation during remnant particle removal, which was also evident from B apolipoprotein studies. Furthermore, unlike in the normal subject transfer of C apolipoprotein radioactivity from triacylglycerol-rich lipoproteins to HDL was greater than that of mass, also suggesting heterogeneity in C apolipoprotein catabolism. The studies show that C apolipoprotein metabolism may be disturbed in severely hypertriglyceridemic subjects: the lack of conservation of these proteins within HDL may exacerbate the degree of hyperlipoproteinemia.