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Alteration of Hepatic Fatty Acid Metabolism After Burn Injury in Pigs
Author(s) -
Martini Wenjun Z.,
Irtun Oivind,
Chinkes David L.,
Rasmussen Blake,
Traber Daniel L.,
Wolfe Robert R.
Publication year - 2001
Publication title -
journal of parenteral and enteral nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.935
H-Index - 98
eISSN - 1941-2444
pISSN - 0148-6071
DOI - 10.1177/0148607101025006310
Subject(s) - medicine , endocrinology , triglyceride , fatty acid , enteral administration , metabolism , beta oxidation , chemistry , parenteral nutrition , cholesterol , biochemistry
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‐ 13 C 16 ‐palmitate in order to quantify hepatic FA kinetics and oxidation. Results: Liver triglyceride (TG) content was elevated from 162 ± 16 (control) to 297 ± 28 μmol 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 μmol/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. (Journal of Parenteral and Enteral Nutrition 25:310–316, 2001)