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 micromol 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 micromol/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.
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 micromol 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 micromol/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.
Authors: Christian Sommerhalder; Elizabeth Blears; Andrew J Murton; Craig Porter; Celeste Finnerty; David N Herndon Journal: Curr Probl Surg Date: 2019-11-11 Impact factor: 1.909
Authors: Jong O Lee; Gerd G Gauglitz; David N Herndon; Hal K Hawkins; Stefanie C Halder; Marc G Jeschke Journal: J Surg Res Date: 2010-11-04 Impact factor: 2.192
Authors: Melanie G Cree; Bradley R Newcomer; David N Herndon; Ting Qian; Dayoung Sun; Beatrice Morio; Jennifer J Zwetsloot; G Lynis Dohm; Ricki Y Fram; Ronald P Mlcak; Asle Aarsland; Robert R Wolfe Journal: Nutr Metab (Lond) Date: 2007-04-23 Impact factor: 4.169