Hepatic glutamine transporter activation in burn injury: Role of amino acids and phosphatidylinositol-3-kinase

Timothy M. Pawlik, Rüdiger Lohmann, Wiley W. Souba, Barrie P. Bode

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Burn injury elicits a marked, sustained hypermetabolic state in patients characterized by accelerated hepatic amino acid metabolism and negative nitrogen balance. The transport of glutamine, a key substrate in gluconeogenesis and ureagenesis, was examined in hepatocytes isolated from the livers of rats after a 20% total burn surface area full-thickness scald injury. A latent and profound two- to threefold increase in glutamine transporter system N activity was first observed after 48 h in hepatocytes from injured rats compared with controls, persisted for 9 days, and waned toward control values after 18 days, corresponding with convalescence. Further studies showed that the profound increase was fully attributable to rapid posttranslational transporter activation by amino acid-induced cell swelling and that this form of regulation may be elicited in part by glucagon. The phosphatidylinositol-3-kinase (PI3K) inhibitors wortmannin and LY-294002 each significantly attenuated transporter stimulation by amino acids. The data suggest that PI3K-dependent system N activation by amino acids may play an important role in fueling accelerated hepatic nitrogen metabolism after burn injury.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number4 41-4
StatePublished - Apr 2000
Externally publishedYes


  • Cell volume
  • Glucagon
  • Liver
  • Signal transduction

ASJC Scopus subject areas

  • Gastroenterology
  • Physiology
  • Physiology (medical)


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