Cerebral energy metabolism in Hepatic Encephalopathy and hyperammonemia

K. V Rama Rao, Michael D Norenberg

Research output: Contribution to journalArticle

102 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)67-78
Number of pages12
JournalMetabolic Brain Disease
Volume16
Issue number1-2
DOIs
StatePublished - Nov 26 2001

Fingerprint

Hyperammonemia
Hepatic Encephalopathy
Ammonia
Energy Metabolism
Glutamine
Oxidative stress
Glycolysis
Electron Transport
Metabolites
Nervous System Diseases
Metabolism
Astrocytes
Liver
Neurotransmitter Agents
Liver Diseases
Permeability
Oxidative Stress
Morbidity
Mortality

Keywords

  • Ammonia
  • Astrocytes
  • Energy metabolism
  • Hepatic encephalopathy
  • Mitochondrial permeability transition
  • Mitrochondria

ASJC Scopus subject areas

  • Clinical Neurology
  • Biochemistry
  • Neuroscience(all)

Cite this

Cerebral energy metabolism in Hepatic Encephalopathy and hyperammonemia. / Rao, K. V Rama; Norenberg, Michael D.

In: Metabolic Brain Disease, Vol. 16, No. 1-2, 26.11.2001, p. 67-78.

Research output: Contribution to journalArticle

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