Contribution of dietary arginine to nitrogen utilisation and excretion in juvenile sea bass ( Dicentrarchus labrax) fed diets differing in protein source

• Published in: Comparative biochemistry and physiology. A, Comparative physiology Comparative physiology, 2007-05, Vol.147 (1), p.179-188
• Main Authors: Tulli, F., Vachot, C., Tibaldi, E., Fournier, V., Kaushik, S.J.
• Format: Article
• Language: English
• Subjects: Ammonia - blood; Animals; Arginase; Arginase - metabolism; Arginine; Arginine - administration & dosage; Arginine - pharmacology; Bass - growth & development; Bass - metabolism; Biochemistry, Molecular Biology; Dicentrarchus labrax; Diet; Dietary Proteins - administration & dosage; Dietary Proteins - pharmacology; Excretion; Feeding Behavior - drug effects; Fish Proteins - metabolism; Glutamate Dehydrogenase - metabolism; Kinetics; Life Sciences; Lipid Metabolism - drug effects; Liver - drug effects; Liver - enzymology; Marine; Nitrogen - blood; Nitrogen - metabolism; Ornithine Carbamoyltransferase - metabolism; Sea bass; Urea; Urea - blood; Uric Acid - blood
• ISSN: 1095-6433; 0300-9629; 1531-4332
• DOI: 10.1016/j.cbpa.2006.12.036

The role of dietary arginine in affecting nitrogen utilisation and excretion was studied in juvenile European sea bass ( Dicentrarchus labrax) fed for 72 days with diets differing in protein sources (plant protein-based (PM) and fish-meal-based (FM)). Fish growth performance and nitrogen utilisation revealed that dietary Arg surplus was beneficial only in PM diets. Dietary Arg level significantly affected postprandial plasma urea concentrations. Hepatic arginase activity increased ( P < 0.05) in response to dietary Arg surplus in fish fed plant protein diets; conversely ornithine transcarbamylase activity was very low and inversely related to arginine intake. No hepatic carbamoyl phosphate synthetase III activity was detected. Dietary arginine levels did not affect glutamate dehydrogenase activity. A strong linear relationship was found between liver arginase activity and daily urea-N excretion. Dietary Arg excess reduced the proportion of total ammonia nitrogen excreted and increased the contribution of urea-N over the total N excretion irrespective of dietary protein source. Plasma and excretion data combined with enzyme activities suggest that dietary Arg degradation via hepatic arginase is a major pathway for ureagenesis and that ornithine-urea cycle is not completely functional in juvenile sea bass liver.