Glutamine in the pathogenesis of acute hepatic encephalopathy

Kakulavarapu V. Rama Rao, Arumugam R. Jayakumar, Michael D. Norenberg

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)575-580
Number of pages6
JournalNeurochemistry International
Issue number4
StatePublished - Sep 2012
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Cellular and Molecular Neuroscience
  • Cell Biology


  • Acute liver failure
  • Ammonia
  • Astrocytes
  • Glutamine
  • Hepatic encephalopathy
  • Histidine
  • Mitochondria
  • Mitochondrial permeability transition
  • Oxidative stress


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