Metabolic Brain Disease

, Volume 16, Issue 1–2, pp 67–78

Cerebral Energy Metabolism in Hepatic Encephalopathy and Hyperammonemia

Article

DOI: 10.1023/A:1011666612822

Cite this article as:
Rao, K.R. & Norenberg, M. Metab Brain Dis (2001) 16: 67. doi:10.1023/A:1011666612822

Abstract

Hepatic encephalopathy (HE) is an important cause of morbidity and mortality in patients with severe liver disease. Although the molecular basis for the neurological disorder in HE remains elusive, elevated ammonia and its chief metabolite glutamine are believed to be important factors responsible for altered cerebral functions, including multiple neurotransmitter system(s) failure, altered bioenergetics, and more recently oxidative stress. Accumulated evidence suggests that direct interference of ammonia at several points in cerebral energy metabolism, including glycolysis, TCA cycle, and the electron transport chain, could lead to energy depletion. Additionally, recent studies from our laboratory have invoked the possibility that ammonia and glutamine may induce the mitochondrial permeability transition in astrocytes, a process capable of causing mitochondrial dysfunction. Altered mitochondrial metabolism appears to be an important mechanism responsible for the cerebral abnormalities associated with HE and other hyperammonemic states.

Astrocytes ammonia mitrochondria mitochondrial permeability transition energy metabolism hepatic encephalopathy 

Copyright information

© Plenum Publishing Corporation 2001

Authors and Affiliations

  1. 1.Laboratory of NeuropathologyVeterans Administration Medical CenterUSA
  2. 2.Departments of Pathology and Biochemistry and Molecular BiologyUniversity of Miami School of MedicineMiami

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