STIMULATION OF RAT HEPATIC AMINO-ACID-TRANSPORT BY BURN INJURY

Burn injury accelerates hepatic amino acid metabolism, but the role of transmembrane substrate delivery in this response has not been invest igated. We therefore studied the effects of cutaneous scald injury on the Na+-dependent transport of glutamine and alanine in isolated rat l iver plasma membrane vesicles. Scald injury resulted in liver damage a nd a 1.4- to 2.3-fold and 1.5- to 2.8-fold stimulation of hepatic tran sport rates for glutamine and alanine, respectively, proportional to t he total burned surface area (TBSA) after 24 hours. Enhanced uptake of glutamine and alanine was attributable to increases in the maximum ve locity (V-max) of system N and system A activities, respectively. Hepa tic amino acid transport activity remained elevated in vesicles from b urned animals after 72 hours, but the degree of stimulation (1.3- to 1 .7-fold for glutamine and 1.3- to 1.6-fold for alanine) was less than that observed 24 hours after thermal injury. Liver function tests retu rned to control values after 72 hours as well, indicating rectificatio n of hepatic damage. In contrast to the induction of hepatic system A and system N activity in catabolic states such as cancer and endotoxem ia, further studies showed that tumor necrosis factor (TNF) failed to play a significant role in burn-stimulated amino acid transport rates. When combined with plasma liver enzyme profiles, early transient hepa tic amino acid transporter stimulation may support amino acid-dependen t pathways involved in the repair of burn-dependent hepatic damage. Co pyright (C) 1998 by W.B. Saunders Company.