Release, oxidation, and reesterification of fatty acids from infused triglycerides: Effect of heparin

We have investigated the effects of heparin on rates of fatty acid (FA) release, oxidation, and reesterification from intravenously (IV) infused triglycerides (TGs) during euglycemic (4.7 mmol . L(-1)) hyperinsulinemia (similar to 450 pmol . L(-1)). Four healthy men (aged 31 +/- 3 years; body mass index, 26.1 +/- 0.9 kg/m(2)) received IV TGs (1.02 mmol TG . kg(-1). 4 h(-1)), four other men (aged 24.3 +/- 2.8 years; body mass index, 24.7 +/- 1.7 kg/m(2)) received TGs plus heparin (200-U bolus followed by 0.4 U . kg(-1). min(-1)), and nine men and one woman (aged 28.8 +/- 2.3 years; body mass index, 23.1 +/- 0.9 kg/m(2)) received saline (controls). Heparin increased lipolysis from infused TGs (to 1.0 +/- 0.1 from 0.3 +/- 0.1 mmol . kg(-1). 4 h(-1), P <.01), increased plasma free fatty acids ([FFA] to 737 +/- 32 from 597 +/- 136 mu mol . L(-1), P <.05), and increased FA reesterification (to 0.84 +/- 0.14 from 0.18 +/- 0.12 mmol . kg(-1). 4 h(-1), P <.02), but had no effect on FA oxidation (0.13 +/- 0.02 v 0.12 +/- 0.04 mmol . kg(-1). 4 h(-1)) or net energy gain (167 +/- 42 v 243 +/- 79 kJ . 4 h(-1)). In summary, addition of heparin (1) increased lipolysis (to similar to 98% from similar to 29%) and reesterification (to similar to 82% from similar to 17%) of infused TG, but had no significant effects on fat oxidation (similar to 12%) and net energy gain. We conclude that heparin accelerated removal of infused lipid from the blood and its deposition into endogenous fat depots. Since the doses of heparin and insulin used in this study were higher than those generally used in total parenteral nutrition protocols, our results may not be strictly applicable to the usual clinical situation. Copyright (C) 1995 by W.B. Saunders Company