Abstract
Guanidino compounds are considered to be one of the metabolic products of protein catabolism. Serum concentrations of some guanidino compounds especially methylguanidine (MG)1 and guanidinosuccinic acid (GSA)2 are increased in the uremic state. Recently, MG and GSA were found to have uremic toxicity in vitro3. Giovanetti4, et al., for example, brought out many uremic symptoms in normal dogs by repeatedly injecting MG until the MG concentration reached the uremic state. Cohen5 proposed the metabolic pathway of MG. He suggested that the metabolic origin of MG is mainly creatine and partially of arginine (Arg). The present authors have also suggested that there might be two metabolic origins of MG6. One is possibly Arg itself (or the metabolites of arginine); the other is creatinine (Cr). The present study aims to clarify the metabolic precursor of guanidino compounds, especially MG (Fig.l).
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Mikami, H. et al. (1982). Metabolic Pathway of Guanidino Compounds in Chronic Renal Failure. In: Lowenthal, A., Mori, A., Marescau, B. (eds) Urea Cycle Diseases. Advances in Experimental Medicine and Biology, vol 153. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-6903-6_55
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DOI: https://doi.org/10.1007/978-1-4757-6903-6_55
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