Background: The primary goal of this study was to investigate hepatic fatty
acid (FA) metabolism after severe thermal injury. Methods: Sixteen pigs we
re divided into control (n = 8) and burn (n = 8, with 40% full thickness to
tal body surface area burned) groups. Catheters were inserted in the right
common carotid artery, portal vein, and hepatic vein for blood sampling. Fl
ow probes were placed around the hepatic artery and portal vein for blood f
low 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-
C-13(16)-palmitate in order to quantify hepatic FA kinetics and oxidation.
Results: Liver triglyceride (TG) content was elevated from 162 +/- 16 (cont
rol) to 297 +/- 28 mu mol TG/g dry liver wt. (p < .05). Hepatic FA uptake a
nd oxidation were similar between the 2 groups, as were malonyl- coenzyme A
(CoA) levels and activities of acetyl-CoA carboxylase and adenosine monoph
osphate (AMP)-activated protein kinase. In contrast, incorporation of plasm
a-free fatty acids into hepatic TG was elevated (p < .05) and very low dens
ity lipoprotein TG (VLDL-TG) secretion was decreased from 0.17 +/- 0.02 (co
ntrol) to 0.03 +/- 0.01 mu mol/kg per minute in burned pigs (p < .05). Conc
lusions: The accumulation of hepatic TG in burned animals is due to inhibit
ion of VLDL-TG secretion and to increased synthesis of hepatic TG. Fatty ac
ids are not channeled to TG because of impaired oxidation.