Kohno M, Fujii T, Hirayama C
Second Department of Internal Medicine, Tottori University School of Medicine, Yonago, Japan.
Biochem Med Metab Biol. 1990 Jun;43(3):201-13. doi: 10.1016/0885-4505(90)90026-w.
Following a single oral dose of 10 mg/kg of [15N]glycine, plasma [15N]glycine kinetics and urinary 15N excretion were measured in 12 cirrhosis patients and in 6 control subjects. Cirrhosis patients were divided into two groups of 6 patients with and without a history of hepatic encephalopathy designated as group II and group I, respectively. Thirty minutes after oral administration of labeled glycine, the plasma concentration of [15N]glycine was significantly higher in both cirrhosis groups than that in the control group (P less than 0.05 and P less than 0.01). The elimination constant of plasma [15N]glycine slightly decreased in group II, but not significantly. Urinary 15N excretion did not differ among the three groups, but the rate of urinary ammonia 15N in urinary 15N was significantly increased in group II (P less than 0.05). The whole-body protein flux did not differ among the three groups, but whole-body protein breakdown was significantly increased in group II cirrhosis patients (P less than 0.05). These findings indicated that the kinetics of glycine were substantially altered in severe cirrhosis patients. Because hepatic uptake and oxidation of glycine was well maintained even in group II, increased endogenous protein breakdown seemed to be responsible for hyperglycinemia and also for the negative nitrogen balance seen in this group.
在12名肝硬化患者和6名对照受试者中，口服单剂量10mg/kg的[15N]甘氨酸后，测定了血浆[15N]甘氨酸动力学和尿15N排泄。肝硬化患者分为两组，每组6例，分别有和无肝性脑病病史，分别指定为II组和I组。口服标记甘氨酸30分钟后，两个肝硬化组的血浆[15N]甘氨酸浓度均显著高于对照组（P<0.05和P<0.01）。II组血浆[15N]甘氨酸的消除常数略有下降，但无显著差异。三组之间的尿15N排泄无差异，但II组尿15N中的尿氨15N率显著增加（P<0.05）。三组之间的全身蛋白质通量无差异，但II组肝硬化患者的全身蛋白质分解显著增加（P<0.05）。这些发现表明，严重肝硬化患者甘氨酸的动力学发生了显著改变。由于即使在II组中甘氨酸的肝脏摄取和氧化也保持良好，内源性蛋白质分解增加似乎是导致高甘氨酸血症的原因，也是该组中负氮平衡的原因。
