Effect of heparin-stimulated plasma lipolytic activity on VLDL APO B subclass metabolism in normal subjects

Heparin given intravenously enhances lipolysis, although fasting lipids are not markedly altered in long-term administration. In the present study we investigated heparin-induced acute perturbation of VLDL subclass metabolism. Eight men were examined during a control study and during an 8.5 h infusion of heparin. 2H3-leucine was used as tracer and kinetic constants derived using a non-steady-state model. Heparin infusion increased both plasma lipoprotein and hepatic lipase activity and raised plasma FFAs two-fold (P<0.001). The fractional catabolic rate (FCR) of VLDL1 apo B increased on heparin (25.7±4.2 and 10.8±1.7 pools/d, heparin vs. control, P<0.02). The FCR of VLDL2 apo B increased to 12.6±1.9 pools/d on heparin vs. 8.8±1.1 pools/d during the control (NS). Total VLDL apo B production was not significantly changed (824±45 and 692±91 mg/d, heparin vs. control, NS). We conclude that during heparin infusion, the catabolism of especially large triglyceride-rich VLDL1 apo B is greatly increased. However, although the FFA levels were high during the heparin study, the production of total VLDL apo B did not rise. These findings are consistent with the known action of heparin on lipoprotein lipase but indicate that acute increase in plasma FFA levels does not lead to a rise in VLDL apo B production.