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 approximately 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.
Aarsland
A
A
The Metabolism Unit, Shriners Burns Institute, Galveston, TX 77551, USA.
Chinkes
D L
DL
Sakurai
Y
Y
Nguyen
T T
TT
Herndon
D N
DN
Wolfe
R R
RR
D000293:Adolescent; D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D002056:Burns / Q000628:therapy*; D002241:Carbohydrates / Q000008:administration & dosage; D004032:Diet; D004734:Energy Metabolism / Q000502:physiology; D005227:Fatty Acids / Q000097:blood; D005260:Female; D005934:Glucagon / Q000097:blood; D005947:Glucose / Q000008:administration & dosage; D006801:Humans; D007328:Insulin / Q000097:blood / Q000627:therapeutic use*; D019344:Lactic Acid / Q000097:blood; D050356:Lipid Metabolism; D008074:Lipoproteins / Q000097:blood; D008099:Liver / Q000378:metabolism*; D008297:Male; D014280:Triglycerides / Q000097:blood*
D001786:Blood Glucose; D002241:Carbohydrates; D005227:Fatty Acids; D007328:Insulin; D008074:Lipoproteins; D014280:Triglycerides; D019344:Lactic Acid; D005934:Glucagon; D005947:Glucose