Glycine and hyperammonemia: potential target for the treatment of hepatic encephalopathy
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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.
KeywordsAmmonia Glutamine Glycine L-ornithine-phenylacetate (OP) Phenylacetylglycine
Glycine cleavage system
Acute liver failure
- NMDA receptor
Compliance with ethical standards
Conflict of interest statement
None of the authors have anything to disclose.
- McGuire BM, Zupanets IA, Lowe ME, Xiao X, Syplyviy VA, Monteleone J, Gargosky S, Dickinson K, Martinez A, Mokhtarani M, Scharschmidt BF (2010) Pharmacology and safety of glycerol phenylbutyrate in healthy adults and adults with cirrhosis. Hepatology 51(6):2077–2085CrossRefPubMedPubMedCentralGoogle Scholar
- Misel ML, Gish RG, et al. (2013) Sodium benzoate for treatment of hepatic encephalopathy. Gastroenterol Hepatol (N Y) 9(4):219–227Google Scholar
- Vilstrup H, Amodio P, Bajaj J, Cordoba J, Ferenci P, Mullen KD, Weissenborn K, Wong P (2014) Hepatic encephalopathy in chronic liver disease: 2014 practice guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the liver. Hepatology 60(2):715–735CrossRefPubMedGoogle Scholar