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Titolo:
Intrahepatic amino acid and glucose metabolism in a D-galactosamine-induced rat liver failure model
Autore:
Arai, K; Lee, K; Berthiaume, F; Tompkins, RG; Yarmush, ML;
Indirizzi:
Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med,Surg Serv, Boston, MA 02114 USA Harvard Univ Boston MA USA 02114 Engn Med,Surg Serv, Boston, MA 02114 USA Shriners Hosp Children, Boston, MA USA Shriners Hosp Children Boston MA USA iners Hosp Children, Boston, MA USA
Titolo Testata:
HEPATOLOGY
fascicolo: 2, volume: 34, anno: 2001,
pagine: 360 - 371
SICI:
0270-9139(200108)34:2<360:IAAAGM>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
FULMINANT HEPATIC-FAILURE; ISOLATED-PERFUSED LIVER; NITROGEN-METABOLISM; BRAIN EDEMA; CLINICAL-EXPERIENCE; CIRRHOTIC RATS; CEREBRAL EDEMA; ENCEPHALOPATHY; AMMONIA; PLASMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
69
Recensione:
Indirizzi per estratti:
Indirizzo: Yarmush, ML Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Engn Med,Surg Serv, GRB1401,55 Fruit St, Boston, MA 02114 USA Harvard Univ GRB 1401,55Fruit St Boston MA USA 02114 2114 USA
Citazione:
K. Arai et al., "Intrahepatic amino acid and glucose metabolism in a D-galactosamine-induced rat liver failure model", HEPATOLOGY, 34(2), 2001, pp. 360-371

Abstract

A better understanding of the hepatic metabolic pathways affected by fulminant hepatic failure (FHF) would help develop nutritional support and othernonsurgical medical therapies for FHF. We used an isolated perfused liver system in combination with a mass-balance model of hepatic intermediary metabolism to generate a comprehensive map of metabolic alterations in the liver in FHF. To induce FHF, rats were fasted for 36 hours, during which they received 2 D-galactosamine injections. The livers were then perfused for 60minutes via the portal vein with amino acid-supplemented Eagle minimal essential medium containing 3% wt/vol bovine serum albumin and oxygenated with95% O-2/5% CO2- Control rats were fasted for 36 hours with no other treatment before perfusion. FHF rat livers exhibited reduced amino acid uptake, aswitch from gluconeogenesis to glycolysis, and a decrease in urea synthesis, but no change in ammonia consumption compared with normal fasted rat livers. Mass-balance analysis showed that hepatic glucose synthesis was inhibited as a result of a reduction in amino acid entry into the tricarboxylic acid cycle by anaplerosis. Furthermore, FHF inhibited intrahepatic aspartatesynthesis, which resulted in a 50% reduction in urea cycle flux. Urea synthesis by conversion of exogenous arginine to ornithine was unchanged. Ammonia removal was quantitatively maintained by glutamine synthesis from glutamate and a decrease in the conversion of glutamate to a-ketoglutarate. Mass-balance analysis of hepatic metabolism will be useful in characterizing changes during FHF, and in elucidating the effects of nutritional supplements and other treatments on hepatic function.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 00:04:29