Orita Y, Tsubakihara Y, Ando A, Nakata K, Takamitsu Y, Fukuhara Y, Abe H
Nephron. 1978;22(4-6):328-36. doi: 10.1159/000181471.
The metabolic pathway of methylguanidine (MG) is mainly speculated from the change in urinary excretion of MG in the arginine (Arg)-injected normal rat, the creatinine (Cr)-injected normal rat, and the Arg-injected uremic rat. 15N-Arg was ingested to 2 uremic patients. Arg administration resulted in marked increase in urinary MG excretion both in the uremic rat and patient, but not in the normal rat. In the first phase of the 15N-Arg ingestion experiment, a rapid rise of 15N atom percent excess of urinary MG was observed in the uremic patient. In the second phase of this study, after 24 h of 15N-Arg ingestion, the 15N atom percent excess of urinary Cr and that of MG closely paralleled. These findings imply that there might be two metabolic origins of MG: one is a formation of MG from Arg itself or an Arg metabolite other than Cr, the other a pathway producing MG via Cr. The former is compatible with the hypothesis by Cohen.
甲基胍（MG）的代谢途径主要是根据向正常大鼠注射精氨酸（Arg）、向正常大鼠注射肌酐（Cr）以及向尿毒症大鼠注射Arg后尿中MG排泄量的变化推测出来的。给2例尿毒症患者摄入15N-Arg。给予Arg后，尿毒症大鼠和患者尿中MG排泄量均显著增加，但正常大鼠未出现这种情况。在15N-Arg摄入实验的第一阶段，尿毒症患者尿中MG的15N原子超量百分比迅速上升。在本研究的第二阶段，摄入15N-Arg 24小时后，尿中Cr和MG的15N原子超量百分比密切平行。这些发现表明，MG可能有两个代谢来源：一个是由Arg本身或除Cr之外的Arg代谢产物形成MG，另一个是通过Cr产生MG的途径。前者与科恩提出的假说相符。
