Yokota S, Kumano K, Hyodo T, Sakai T, Izumi G, Hashimoto A, Shibata K, Wang H
Kidney Center, Kitasato University Hospital, Kanagawa, Japan.
Adv Perit Dial. 1998;14:195-9.
There are indications that advanced glycosylation end-products (AGEs) may affect in some manner the functions of the peritoneum. Only a few reports discuss the actual generation of glycosylated proteins and the intraperitoneal kinetics involved during continuous ambulatory peritoneal dialysis (CAPD). To demonstrate the formation of AGEs and their time-courses in peritoneal dialysis (PD) effluents, measurements were made of furosine, carboxymethyl lysine (CML), and pentosidine as glycosylation markers in vitro and in vivo using PD effluents obtained every 2 hours for up to 8 hours from 3 nondiabetic CAPD patients. Furosine and CML were found to be generated relatively early (within 6 hours), and their de novo formation was markedly enhanced subsequent to glucose addition. Furosine and CML production increased in proportion to glucose concentration. Pentosidine production did not change with time for up to 24 hours, and was not induced by glucose during this period. Carboxymethyl lysine production appeared to be suppressed in vitro with the addition of serum protein. Furosine in the intraperitoneal dialysate was initially the same as that in the plasma, but increased to twice as much in just 2 hours in vivo. Production of CML increased, but apparently was suppressed with leakage of plasma protein into the dialysate; this possibly may have been due to dilutional or antiglycation effects in the plasma. No stimulation of pentosidine production could be detected in the intraperitoneal dialysate even at 8 hours. The initiation of glycosylation of peritoneal proteins, with generation of furosine and CML but not pentosidine, is clearly shown by the present results to occur relatively early in the intraperitoneal dialysate, i.e., within a matter of hours.
有迹象表明，晚期糖基化终产物（AGEs）可能会以某种方式影响腹膜的功能。仅有少数报告讨论了糖基化蛋白的实际生成情况以及持续非卧床腹膜透析（CAPD）期间的腹膜内动力学。为了证明腹膜透析（PD）流出液中AGEs的形成及其时间进程，我们使用从3名非糖尿病CAPD患者身上每2小时获取一次、长达8小时的PD流出液，在体外和体内对作为糖基化标记物的呋喃果糖、羧甲基赖氨酸（CML）和戊糖苷进行了测量。结果发现，呋喃果糖和CML相对较早生成（6小时内），添加葡萄糖后其从头形成显著增强。呋喃果糖和CML的生成量与葡萄糖浓度成正比。戊糖苷的生成在长达24小时内随时间没有变化，在此期间也未被葡萄糖诱导。添加血清蛋白后，体外羧甲基赖氨酸的生成似乎受到抑制。腹膜内透析液中的呋喃果糖最初与血浆中的相同，但在体内仅2小时就增加到原来的两倍。CML的生成增加，但显然随着血浆蛋白漏入透析液而受到抑制；这可能是由于血浆中的稀释或抗糖基化作用。即使在8小时时，腹膜内透析液中也未检测到戊糖苷生成的刺激作用。本研究结果清楚地表明，腹膜蛋白糖基化的起始，即呋喃果糖和CML而非戊糖苷的生成，在腹膜内透析液中相对较早发生，即在数小时内。
