title: Brain energy metabolism and mitochondrial dysfunction in acute and chronic hepatic encephalopathy.
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.
authors: Department of Pathology, University of Miami Miller School of Medicine, Miami, FL 33125, United States.
authors: Kakulavarapu V
authors: KV
authors: Rama Rao
authors: Michael D
authors: MD
authors: Norenberg
mesh_terms: D000208:Acute Disease; D000641:Ammonia / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D002908:Chronic Disease; D002952:Citric Acid Cycle; D004734:Energy Metabolism; D006019:Glycolysis; D006501:Hepatic Encephalopathy / Q000378:metabolism*; D006801:Humans; D019344:Lactic Acid / Q000378:metabolism; D008928:Mitochondria / Q000502:physiology*; D015538:Nitrosation; D010085:Oxidative Phosphorylation; D018384:Oxidative Stress; D010539:Permeability
chemical_list: D019344:Lactic Acid; D000641:Ammonia