Glutamine in the pathogenesis of acute hepatic encephalopathy |
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Authors: | Rama Rao Kakulavarapu V Jayakumar Arumugam R Norenberg Michael D |
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Institution: | Department of Pathology, University of Miami Miller School of Medicine, Miami, FL 33125, United States. |
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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. |
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Keywords: | Acute liver failure Ammonia Astrocytes Glutamine Hepatic encephalopathy Histidine Mitochondria Mitochondrial permeability transition Oxidative stress |
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