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 (approximately 450 pmol.L-1). Four healthy men (aged 31 +/- 3 years; body mass index, 26.1 +/- 0.9 kg/m2) received i.v. 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/m2) 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/m2) 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 mumol.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 o n FA oxidation (0.13 +/- 0.02 v 0.12 +/- 0.04 mmol.kg-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 approximately 98% from approximately 29%) and reesterification (to approximately 82% from approximately 17%) of infused TG, but had no significant effects on fat oxidation (approximately 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.