Alteration of hepatic fatty acid metabolism after burn injury in pigs

W. Z. Martini, O. Irtun, D. L. Chinkes, Blake Rasmussen, D. L. Traber, R. R. Wolfe

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background: The primary goal of this study was to investigate hepatic fatty acid (FA) metabolism after severe thermal injury. Methods: Sixteen pigs were divided into control (n = 8) and burn (n = 8, with 40% full thickness total body surface area burned) groups. Catheters were inserted in the right common carotid artery, portal vein, and hepatic vein for blood sampling. Flow probes were placed around the hepatic artery and portal vein for blood flow measurements. Animals were given pain medication and sedated until the tracer study on day 4 after burn. The pigs were infused for 4 hours with U-13C16-palmitate in order to quantify hepatic FA kinetics and oxidation. Results: Liver triglyceride (TG) content was elevated from 162 ± 16 (control) to 297 ± 28 uμmol TG/g dry liver wt. (p < .05). Hepatic FA uptake and oxidation were similar between the 2 groups, as were malonyl-coenzyme A (CoA) levels and activities of acetyl-CoA carboxylase and adenosine monophosphate (AMP)-activated protein kinase. In contrast, incorporation of plasma-free fatty acids into hepatic TG was elevated (p < .05) and very low density lipoprotein TG (VLDL-TG) secretion was decreased from 0.17 ± 0.02 (control) to 0.03 ± 0.01 uμmol/kg per minute in burned pigs (p < .05). Conclusions: The accumulation of hepatic TG in burned animals is due to inhibition of VLDL-TG secretion and to increased synthesis of hepatic TG. Fatty acids are not channeled to TG because of impaired oxidation.

Original languageEnglish (US)
Pages (from-to)310-316
Number of pages7
JournalJournal of Parenteral and Enteral Nutrition
Volume25
Issue number6
StatePublished - 2001
Externally publishedYes

Fingerprint

burns (injuries)
fatty acid metabolism
Swine
Fatty Acids
liver
Triglycerides
swine
triacylglycerols
Liver
Wounds and Injuries
Hepatic Veins
portal vein
Portal Vein
very low density lipoprotein
oxidation
fatty acids
malonyl coenzyme A
Malonyl Coenzyme A
hepatic artery
Acetyl-CoA Carboxylase

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Martini, W. Z., Irtun, O., Chinkes, D. L., Rasmussen, B., Traber, D. L., & Wolfe, R. R. (2001). Alteration of hepatic fatty acid metabolism after burn injury in pigs. Journal of Parenteral and Enteral Nutrition, 25(6), 310-316.

Alteration of hepatic fatty acid metabolism after burn injury in pigs. / Martini, W. Z.; Irtun, O.; Chinkes, D. L.; Rasmussen, Blake; Traber, D. L.; Wolfe, R. R.

In: Journal of Parenteral and Enteral Nutrition, Vol. 25, No. 6, 2001, p. 310-316.

Research output: Contribution to journalArticle

Martini, WZ, Irtun, O, Chinkes, DL, Rasmussen, B, Traber, DL & Wolfe, RR 2001, 'Alteration of hepatic fatty acid metabolism after burn injury in pigs', Journal of Parenteral and Enteral Nutrition, vol. 25, no. 6, pp. 310-316.
Martini, W. Z. ; Irtun, O. ; Chinkes, D. L. ; Rasmussen, Blake ; Traber, D. L. ; Wolfe, R. R. / Alteration of hepatic fatty acid metabolism after burn injury in pigs. In: Journal of Parenteral and Enteral Nutrition. 2001 ; Vol. 25, No. 6. pp. 310-316.
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AU - Martini, W. Z.

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AU - Traber, D. L.

AU - Wolfe, R. R.

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N2 - Background: The primary goal of this study was to investigate hepatic fatty acid (FA) metabolism after severe thermal injury. Methods: Sixteen pigs were divided into control (n = 8) and burn (n = 8, with 40% full thickness total body surface area burned) groups. Catheters were inserted in the right common carotid artery, portal vein, and hepatic vein for blood sampling. Flow probes were placed around the hepatic artery and portal vein for blood flow measurements. Animals were given pain medication and sedated until the tracer study on day 4 after burn. The pigs were infused for 4 hours with U-13C16-palmitate in order to quantify hepatic FA kinetics and oxidation. Results: Liver triglyceride (TG) content was elevated from 162 ± 16 (control) to 297 ± 28 uμmol TG/g dry liver wt. (p < .05). Hepatic FA uptake and oxidation were similar between the 2 groups, as were malonyl-coenzyme A (CoA) levels and activities of acetyl-CoA carboxylase and adenosine monophosphate (AMP)-activated protein kinase. In contrast, incorporation of plasma-free fatty acids into hepatic TG was elevated (p < .05) and very low density lipoprotein TG (VLDL-TG) secretion was decreased from 0.17 ± 0.02 (control) to 0.03 ± 0.01 uμmol/kg per minute in burned pigs (p < .05). Conclusions: The accumulation of hepatic TG in burned animals is due to inhibition of VLDL-TG secretion and to increased synthesis of hepatic TG. Fatty acids are not channeled to TG because of impaired oxidation.

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