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Erschienen in: Metabolic Brain Disease 6/2016

21.09.2016 | Short Communication

Current state of knowledge of hepatic encephalopathy (part I): newer treatment strategies for hyperammonemia in liver failure

verfasst von: Rune Gangsoy Kristiansen

Erschienen in: Metabolic Brain Disease | Ausgabe 6/2016

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Abstract

Alterations in interorgan metabolism of ammonia play an important role in the onset of hyperammonemia in liver failure. Glutamine synthetase (GS) in muscle is an important target for ammonia removal strategies in hyperammonemia. Ornithine Phenylacetate (OP) is hypothesized to remove ammonia by providing glutamate as a substrate for increased GS activity and hence glutamine production. The newly generated glutamine conjugates with phenylacetate forming phenylacetylglutamine which can be excreted in the urine, providing an excretion pathway for ammonia. We have also shown that OP targets glycine metabolism, providing an additional ammonia reducing effect.
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Metadaten
Titel
Current state of knowledge of hepatic encephalopathy (part I): newer treatment strategies for hyperammonemia in liver failure
verfasst von
Rune Gangsoy Kristiansen
Publikationsdatum
21.09.2016
Verlag
Springer US
Erschienen in
Metabolic Brain Disease / Ausgabe 6/2016
Print ISSN: 0885-7490
Elektronische ISSN: 1573-7365
DOI
https://doi.org/10.1007/s11011-016-9908-9

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