Slower catabolism of apo B48 than of apo B100 in triglyceride-rich lipoproteins during heparin infusions in type 5 hyperlipoproteinemic subjects.

The catabolism of chylomicrons plus remnants and of VLDL was studied in four subjects with type 5 hyperlipoproteinemia. Large triglyceride-rich lipoproteins Sf greater than 60 were labeled with 125I, reinjected, and the removal of radioactivity in apo B48 and in apo B100 was measured before and during intravenous heparin. The constant infusion of heparin stimulated lipolytic activity and accelerated the disappearance of apo B100 radioactivity (VLDL and their remnants) from the Svedberg flotation unit (Sf) greater than 60 fraction by 27%, 33%, 51%, and 55% in the four subjects. However, the removal rate of radioactivity in apo B48 (chylomicrons and their remnants) was unaffected by heparin in three subjects; in the fourth the fall in radioactivity was less in apo B48 than in apo B100. There were corresponding rises with heparin in Sf 12 to 60 apo B48 radioactivity in only one subject. Thus, increased plasma lipolytic activity accelerated chylomicron (remnant) catabolism very much less than of VLDL (remnant) removal of type 5 hyperlipoproteinemic subjects. It suggests that a major defect leading to type 5 hyperlipoproteinemia is failure of chylomicrons to become degraded to the point where the particles can interact optimally with the hepatic chylomicron remnant receptor.