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Metab Brain Dis. 2016 Dec;31(6):1269-1273. Epub 2016 Jun 23.

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

Author information

1
Department of Anesthesiology, Anesthesia and Critical Care Research Group, University Hospital of North Norway and UiT-The Arctic University of Norway, Tromsø, Norway. rune_ga_kri@outlook.com.
2
Department of Anesthesiology, Ålesund Hospital, Helse Møre og Romsdal, 6010, Ålesund, Norway. rune_ga_kri@outlook.com.
3
Hepato-Neuro Laboratory, CRCHUM, Université de Montréal, Montréal, QC, Canada.
4
Department of Anesthesiology, Anesthesia and Critical Care Research Group, University Hospital of North Norway and UiT-The Arctic University of Norway, Tromsø, Norway.

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.

KEYWORDS:

Ammonia; Glutamine; Glycine; L-ornithine-phenylacetate (OP); Phenylacetylglycine

PMID:
27339764
DOI:
10.1007/s11011-016-9858-2
[Indexed for MEDLINE]

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