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Published in: Metabolic Brain Disease 6/2016

01-12-2016 | Original Article

Glycine and hyperammonemia: potential target for the treatment of hepatic encephalopathy

Authors: Rune Gangsøy Kristiansen, Christopher F. Rose, Lars Marius Ytrebø

Published in: Metabolic Brain Disease | Issue 6/2016

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Abstract

Hepatic encephalopathy (HE) is a neuropsychiatric disorder caused by hepatic dysfunction. Numerous studies dictate that ammonia plays an important role in the pathogenesis of HE, and hyperammonemia can lead to alterations in amino acid homeostasis. Glutamine and glycine are both ammoniagenic amino acids that are increased in liver failure. Modulating the levels of glutamine and glycine has shown to reduce ammonia concentration in hyperammonemia. Ornithine Phenylacetate (OP) has consistently been shown to reduce arterial ammonia levels in liver failure by modulating glutamine levels. In addition to this, OP has also been found to modulate glycine concentration providing an additional ammonia removing effect. Data support that glycine also serves an important role in N-methyl D-aspartate (NMDA) receptor mediated neurotransmission in HE. This potential important role for glycine in the pathogenesis of HE merits further investigations.
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Metadata
Title
Glycine and hyperammonemia: potential target for the treatment of hepatic encephalopathy
Authors
Rune Gangsøy Kristiansen
Christopher F. Rose
Lars Marius Ytrebø
Publication date
01-12-2016
Publisher
Springer US
Published in
Metabolic Brain Disease / Issue 6/2016
Print ISSN: 0885-7490
Electronic ISSN: 1573-7365
DOI
https://doi.org/10.1007/s11011-016-9858-2

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