Insulin therapy in burn patients does not contribute to hepatic triglyceride production

Lipid kinetics were studied in six severely burned patients who were treated with a high dose of exogenous insulin plus glucose to promote protein metabolism. The patients were 20±2-yr-old (SD) with 63±8% total body surface area burned. They were studied in a randomized order (a) in the fed state on the seventh day of a control period (C) of continuous high- carbohydrate enteral feeding alone, and (b) on the seventh day of enteral feeding plus exogenous insulin (200 pmol/h = 28 U/h) with extra glucose given as needed to avoid hypoglycemia (I+G). Despite a glucose delivery rate ~ 100% in excess of energy requirements, the following lipid parameters were unchanged: (a) total hepatic VLDL triglyceride (TG) secretion rate (0.165±0.138 [C] vs. 0.154±0.138 mmol/kg · d^-1 [I+G]), (b) plasma TG concentration (1.58±0.66 [C] vs. 1.36±0.41 mmol/liter [I+G]), and (c) plasma VLDL TG concentration (0.68±0.79 [C] vs. 0.67± 0.63 mmol/liter [I+G]). Instead, the high-carbohydrate delivery in conjunction with insulin therapy increased the proportion of de novo-synthesized palmitate in VLDL TG from 13±5% (C) to 34±14% (I+G), with a corresponding decreased amount of palmitate from lipolysis. In association with the doubling of the secretion rate of de novo-synthesized fatty acid (FA) in VLDL TG during insulin therapy (P > 0.5), the relative amount of palmitate and stearate increased from 35±5 to 44±8% and 4±1 to 7±2%, respectively, in VLDL TG, while the relative concentration of oleate and linoleate decreased from 43±5 to 37±6% and 8±4% to 2±2%, respectively. A 15-fold increase in plasma insulin concentration did not change the rate of release of FA into plasma (8.22±2.86 [C] vs. 8.72±6.68 mmol/kg·d^-1 [I+G]. The peripheral release of FA represents a far greater potential for hepatic lipid accumulation in burn patients than the endogenous hepatic fat synthesis, even during excessive carbohydrate intake in conjunction with insulin therapy.