Cerebral energy metabolism in Hepatic Encephalopathy and hyperammonemia

K. V.Rama Rao, M. D. Norenberg

Research output: Contribution to journalReview articlepeer-review

119 Scopus citations


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 (US)
Pages (from-to)67-78
Number of pages12
JournalMetabolic Brain Disease
Issue number1-2
StatePublished - 2001
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Clinical Neurology
  • Cellular and Molecular Neuroscience


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


Dive into the research topics of 'Cerebral energy metabolism in Hepatic Encephalopathy and hyperammonemia'. Together they form a unique fingerprint.

Cite this