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

Asle Aarsland, David L. Chinkes, Yoichi Sakurai, Thuan T. Nguyen, David Herndon, Robert R. Wolfe

Research output: Contribution to journalArticle

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Abstract

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.

Original languageEnglish (US)
Pages (from-to)2233-2239
Number of pages7
JournalJournal of Clinical Investigation
Volume101
Issue number10
StatePublished - May 15 1998

Fingerprint

Triglycerides
Insulin
Palmitates
Liver
Fatty Acids
Carbohydrates
Enteral Nutrition
Lipids
Glucose
Therapeutics
Stearates
Lipolysis
Body Surface Area
Linoleic Acid
Oleic Acid
Hypoglycemia
Fats
very low density lipoprotein triglyceride
Proteins

Keywords

  • Carbohydrate
  • Fat synthesis
  • Lipogenesis
  • Lipolysis
  • Liver

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Aarsland, A., Chinkes, D. L., Sakurai, Y., Nguyen, T. T., Herndon, D., & Wolfe, R. R. (1998). Insulin therapy in burn patients does not contribute to hepatic triglyceride production. Journal of Clinical Investigation, 101(10), 2233-2239.

Insulin therapy in burn patients does not contribute to hepatic triglyceride production. / Aarsland, Asle; Chinkes, David L.; Sakurai, Yoichi; Nguyen, Thuan T.; Herndon, David; Wolfe, Robert R.

In: Journal of Clinical Investigation, Vol. 101, No. 10, 15.05.1998, p. 2233-2239.

Research output: Contribution to journalArticle

Aarsland, A, Chinkes, DL, Sakurai, Y, Nguyen, TT, Herndon, D & Wolfe, RR 1998, 'Insulin therapy in burn patients does not contribute to hepatic triglyceride production', Journal of Clinical Investigation, vol. 101, no. 10, pp. 2233-2239.
Aarsland A, Chinkes DL, Sakurai Y, Nguyen TT, Herndon D, Wolfe RR. Insulin therapy in burn patients does not contribute to hepatic triglyceride production. Journal of Clinical Investigation. 1998 May 15;101(10):2233-2239.
Aarsland, Asle ; Chinkes, David L. ; Sakurai, Yoichi ; Nguyen, Thuan T. ; Herndon, David ; Wolfe, Robert R. / Insulin therapy in burn patients does not contribute to hepatic triglyceride production. In: Journal of Clinical Investigation. 1998 ; Vol. 101, No. 10. pp. 2233-2239.
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abstract = "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.",
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N2 - 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.

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