Abstract
Creatine is formed by the methylation of guanidinoacetic acid (GAA). GAA is formed from arginine and glycine in a reaction catalyzed by glycine amidinotransferase (GAT). In chronic uremic subjects, the creatine level is increased in the plasma and normal in the urine1,2. The cause of the elevated creatine is not entirely clear. Serum GAA levels are elevated and GAA in the urine is decreased in renal failurel,2. The mechanism of these findings is also unknown. The present report describes a study of creatine metabolism in chronic uremic rats. Creatine and GAA levels in plasma, liver and kidney were measured. GAT activity in the kidney was determined. Conversion of L-[guanidino-14C] arginine to creatine, GAA and urea was also measured in the plasma, kidney, liver and muscle.
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References
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© 1985 Springer Science+Business Media New York
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Owada, S., Ozawa, S., Inouchi, M., Kimura, Y., Ishida, M. (1985). A Study of Creatine Metabolism in Chronic Renal Failure Rats. In: Mori, A., Cohen, B.D., Lowenthal, A. (eds) Guanidines. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0752-6_27
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DOI: https://doi.org/10.1007/978-1-4757-0752-6_27
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4757-0754-0
Online ISBN: 978-1-4757-0752-6
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