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HERO ID
2974608
Reference Type
Journal Article
Title
Glutamine in the pathogenesis of acute hepatic encephalopathy
Author(s)
Rama Rao, KV; Jayakumar, AR; Norenberg, MD
Year
2012
Is Peer Reviewed?
1
Journal
Neurochemistry International
ISSN:
0197-0186
EISSN:
1872-9754
Volume
61
Issue
4
Page Numbers
575-580
Language
English
PMID
22285152
DOI
10.1016/j.neuint.2012.01.012
Web of Science Id
WOS:000309623600017
Abstract
Hepatic encephalopathy (HE) is the major neurological disorder associated with liver disease. It presents in chronic and acute forms, and astrocytes are the major neural cells involved. While the principal etiological factor in the pathogenesis of HE is increased levels of blood and brain ammonia, glutamine, a byproduct of ammonia metabolism, has also been implicated in its pathogenesis. This article reviews the current status of glutamine in the pathogenesis of HE, particularly its involvement in some of the events triggered by ammonia, including mitochondrial dysfunction, generation of oxidative stress, and alterations in signaling mechanisms, including activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-κB). Mechanisms by which glutamine contributes to astrocyte swelling/brain edema associated with acute liver failure (ALF) will also be described.
Keywords
Acute liver failure; Ammonia; Astrocytes; Glutamine; Hepatic encephalopathy; Histidine; Mitochondria; Mitochondrial permeability transition; Oxidative stress
Tags
IRIS
•
Ammonia
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