Triglyceride-Rich Lipoproteins

To define the roles, In vivo, of hepatic triglyceride lipase and lipoprotein lipase in the catabolism of trlglyceiide-rlch lipoproteins, we Investigated the relationship between the activities of the above enzymes In postheparin plasma and the fractional removal rates of very low density lipoproteins (VLDL) and VLDL remnant particles. In 22 patients, the fractional removal rates of VLDL and VLDL-remnant particles were determined from analyses of the disappearance of radlolodlnated Sf 60-400 and Sf 12-60 lipoprotein B apoproteln. The maximal activities of hepatic triglyceride lipase and lipoprotein lipase were determined in plasma samples drawn 2-60 minutes after heparln injection (60 U/kg). A positive correlation was observed between the fractional removal rate of VLDL and postheparin plasma lipoprotein lipase activity (r = 0.65). When all 22 patients were considered together, no relationship was demonstrable between remnant fractional removal and postheparin plasma lipoprotein lipase activity. However, humans may be subdivided with respect to the way In which they catabollze remnants. In some, all remnant may be catabollzed to form LDL. In others, some of the remnant may also be directly removed from the circulation. Those subjects In whom previous studies Indicate that all remnant Is converted to LDL demonstrated a positive correlation between remnant fractional removal rate and postheparin plasma lipoprotein lipase activity (n = 8, r = 0.83). No correlations between postheparin plasma hepatic triglyceride lipase activity and any of the fractional removal rates were found. These data are consistent with the following: 1) lipoprotein lipase plays a key regulatory role In the catabolism of trlglycerlde-rich lipoproteins; 2) this role applies only to those catabollc processes involving the formation of particles of higher density VLDL remnants and low density lipoprotein; and 3) hepatic triglyceride lipase plays no rate-limiting role In the catabolism of VLDL or VLDL-remnant particles. (Arteriosclerosis 2: 396-402, September/October 1982)