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...
Gespeichert in:
| Hauptverfasser: | , , |
|---|---|
| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
1999
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| In: |
Current opinion in clinical nutrition & metabolic care
Year: 1999, Jahrgang: 2, Heft: 1, Pages: 47-53 |
| ISSN: | 1473-6519 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://journals.lww.com/co-clinicalnutrition/Fulltext/1999/01000/Amino_acid_metabolism_in_liver_disease.9.aspx
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| Verfasserangaben: | Eggert Holm, Oliver Sedlaczek, Eva Grips |
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| 520 | |a 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. | ||
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