Hepatic glutamine transporter activation in burn injury: role of amino acids and phosphatidylinositol-3-kinase.
Am J Physiol Gastrointest Liver Physiol
; 278(4): G532-41, 2000 Apr.
Article
en En
| MEDLINE
| ID: mdl-10762606
ABSTRACT
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.
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Base de datos:
MEDLINE
Asunto principal:
Quemaduras
/
Proteínas Portadoras
/
Glutamina
/
Hígado
Límite:
Animals
Idioma:
En
Revista:
Am J Physiol Gastrointest Liver Physiol
Asunto de la revista:
FISIOLOGIA
/
GASTROENTEROLOGIA
Año:
2000
Tipo del documento:
Article
País de afiliación:
Estados Unidos