L-alanine plasma levels after oral loads in non-alcoholic liver cirrhosis: relationship with urea extraformation and ammoniogenesis.
In the post-absorptive stage L-alanine is the main source of alpha-amino-nitrogen reaching the liver as glucose precursor. This aminoacid has been used as a measure of urea synthesis capacity in several pathologic conditions, but it has not been employed sistematically in patients with liver cirrhosis. We tried to address this issue by evaluating: a) L-alanine plasma levels, b) urea extraformation (UE), and c) ammoniogenesis after oral L-alanine (0.25 and 0.50 g/kg b wt) in healthy control subjects and in patients with nonalcoholic compensated (Child-Pugh's A class) and decompensated (Child-Pugh's B and C) liver cirrhosis. L-alanine plasma levels after oral load were higher and lasted longer in cirrhotics as compared to controls. Furthermore, after L-alanine oral load, significantly higher ammonia plasma levels were observed in cirrhotics than in controls. Changes in the urea extraformation were comparable in cirrhotics and controls. Both delayed L-alanine elimination from plasma and L-alanine-induced hyperammoniemia were more evident in decompensated cirrhotics and related to L-alanine dose.
Gentile
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Istituto di Medicina Generale e Metodologia Clinica, I Facoltà di Medicina e Chirurgia, Università di Napoli, Italy.
Loguercio
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Russo
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Coltorti
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D000284:Administration, Oral; D000328:Adult; D000409:Alanine / Q000008:administration & dosage / Q000097:blood / Q000493:pharmacokinetics*; D000641:Ammonia / Q000097:blood*; D005260:Female; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood*; D008297:Male; D008875:Middle Aged; D014508:Urea / Q000097:blood*
D000641:Ammonia; D014508:Urea; D000409:Alanine