title: Amino acid metabolism in liver disease.
abstract: The impairment of transsulphuration during methionine degradation in hepatic failure can be counteracted by treatment with S-adenosylmethionine. Regarding the pathogenesis of hepatic encephalopathy, no convincing evidence exists for tryptophan, glutamine or glutamate being involved. Portal-systemic shunting-induced hyperammonaemia may reduce plasma branched-chain amino acids. The glucose effect on urea synthesis does not exist in cirrhosis.
authors.affiliation: Department of Pathophysiology, Medical Clinic I Mannheim, University of Heidelberg, Germany. eggert.holm@urz.uniheidelberg.de
authors.forename: E
authors.initials: E
authors.lastname: Holm
authors.forename: O
authors.initials: O
authors.lastname: Sedlaczek
authors.forename: E
authors.initials: E
authors.lastname: Grips
mesh_terms: D000596:Amino Acids / Q000378:metabolism*; D000597:Amino Acids, Branched-Chain / Q000378:metabolism; D000641:Ammonia / Q000097:blood*; D000818:Animals; D006801:Humans; D008107:Liver Diseases / Q000378:metabolism*; D008715:Methionine / Q000378:metabolism*; D009414:Nerve Growth Factors / Q000378:metabolism; D014364:Tryptophan / Q000378:metabolism; D014508:Urea / Q000378:metabolism
chemical_list: D000596:Amino Acids; D000597:Amino Acids, Branched-Chain; D009414:Nerve Growth Factors; D000641:Ammonia; D014364:Tryptophan; D014508:Urea; D008715:Methionine