Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy

Kakulavarapu V. Rama Rao, Michael D Norenberg

Research output: Contribution to journalArticle

48 Citations (Scopus)

Abstract

One proposed mechanism for acute and chronic hepatic encephalopathy (HE) is a disturbance in cerebral energy metabolism. It also reviews the current status of this mechanism in both acute and chronic HE, as well as in other hyperammonemic disorders. It also reviews abnormalities in glycolysis, lactate metabolism, citric acid cycle, and oxidative phosphorylation as well as associated energy impairment. Additionally, the role of mitochondrial permeability transition (mPT), a recently established factor in the pathogenesis of HE and hyperammonemia, is emphasized. Energy failure appears to be an important pathogenetic component of both acute and chronic HE and a potential target for therapy.

Original languageEnglish
Pages (from-to)697-706
Number of pages10
JournalNeurochemistry International
Volume60
Issue number7
DOIs
StatePublished - Jun 1 2012

Fingerprint

Chronic Brain Damage
Hepatic Encephalopathy
Energy Metabolism
Brain
Hyperammonemia
Citric Acid Cycle
Oxidative Phosphorylation
Glycolysis
Permeability
Lactic Acid

Keywords

  • Ammonia
  • Astrocytes
  • Brain edema
  • Energy metabolism
  • Hepatic encephalopathy
  • Mitochondrial permeability transition
  • Oxidative stress

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

Cite this

Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy. / Rama Rao, Kakulavarapu V.; Norenberg, Michael D.

In: Neurochemistry International, Vol. 60, No. 7, 01.06.2012, p. 697-706.

Research output: Contribution to journalArticle

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