Amino acid metabolism in liver disease.
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.
Holm
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E
Department of Pathophysiology, Medical Clinic I Mannheim, University of Heidelberg, Germany. eggert.holm@urz.uniheidelberg.de
Sedlaczek
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O
Grips
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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
D000596:Amino Acids; D000597:Amino Acids, Branched-Chain; D009414:Nerve Growth Factors; D000641:Ammonia; D014364:Tryptophan; D014508:Urea; D008715:Methionine