The possibility that impaired removal of
lipoprotein triglyceride from the circulation may be a participating factor in the
hypertriglyceridemia of the obese Zucker rat was examined. We found no significant differences in the
heparin-released
lipoprotein lipase (LPL) activities of the adipose tissue, skeletal muscle, and heart (expressed per gram of tissue) from the lean and obese Zucker rats. Furthermore, the kinetic properties of adipose tissue and heart LPL from the lean and obese rats were similar, indicating that the catalytic efficiency of the
enzyme was unaltered in the obese animals. The postheparin plasma LPL activities of lean and obese rats were also similar. However, the postheparin plasma hepatic
triglyceride lipase (H-TGL) activity in the obese rats was elevated. The higher activity of H-TGL could not alleviate the
hypertriglyceridemia in these animals. Since
hypertriglyceridemia in the obese rats could also be due to the hepatic production of
triglyceride-rich
lipoproteins which are resistant to lipolysis, we therefore isolated
very low density lipoproteins (VLDL) from lean and obese rat liver perfusates and examined their degradation by highly purified human milk LPL. Although certain differences were observed in hepatic
VLDL triglyceride fatty acid composition, the kinetic patterns of LPL-catalyzed
triglyceride disappearance from lean and obese rat liver perfusate VLDL were similar. The isolated liver perfusate VLDL contained sufficient
apolipoprotein C-II for maximum lipolysis. These results indicate that impaired lipolysis is not a contributing factor in the genesis of
hypertriglyceridemia in the genetically obese Zucker rat. The hyperlipemic state may be attributed to hypersecretion of hepatic VLDL and consequent saturation of the lipolytic removal of
triglyceride-rich
lipoproteins from the circulation.