Burn injury produces a marked and prolonged hypermetabolic state, which is characterized by accelerated hepatic amino acid metabolism and negative nitrogen balance. The effect of burn injury on hepatocyte transport of glutamine, a key substrate in gluconeogenesis and ureagenesis, was examined following the administration of a full thickness 20% total body surface scald injury. The burn injury was induced in wild-type mice, as well as two types of knockout mice: a CD-14 knockout and an interleukin-6 (IL-6) knockout. In both the wild-type and CD-14 knockout mice a latent and profound 2-fold increase in hepatocyte glutamine transport was seen. In contrast, hepatocytes isolated from IL-6 knockout mice failed to show an induction of glutamine transport after burn injury. Hepatocytes isolated from burned wild-type and CD-14 knockout mice produced significantly higher levels of IL-6 as compared to hepatocytes isolated from sham burned mice. Histologic analysis of skin isolated from wild-type mice showed a robust inflammatory response whereas skin from IL-6 deficient mice showed minimal inflammation and decreased granulation tissue. The results of this study suggest that IL-6 may play a key role in the stimulation of hepatic glutamine transport following burn injury.

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