Adachi Y, Kinne R, Chowdhury J R, Chowdhury N R, Theilmann L, Tran T, Arias I M
Second Department of Internal Medicine, Kinki University School of Medicine, Osaka, Japan.
Gastroenterol Jpn. 1991 Jun;26(3):350-5. doi: 10.1007/BF02781924.
The uptake of bilirubin diglucuronide (BDG) into isolated rat hepatocytes was investigated in order to characterize the mechanism by which bile pigments are transported by the liver. The BDG uptake by hepatocytes was saturable. The uptake was inhibited by bilirubin, sulfobromophthalein, and bilirubin monoglucuronide, but not by taurocholate. The uptake was not affected by replacement of sodium with other cations except for choline. Only when sodium was replaced with choline, was significant decrease in uptake observed. When chloride was replaced with nitrate, BDG uptake decreased, but it was not changed by replacement with sulfate. Metabolic inhibitors did not affect BDG uptake significantly. Thus bile pigments share a common sodium-independent and electrogenic potential-dependent transporter in liver cell membranes. A high concentration of albumin interferes with BDG uptake.
为了阐明肝脏转运胆汁色素的机制，对胆红素二葡萄糖醛酸酯（BDG）进入分离的大鼠肝细胞的摄取情况进行了研究。肝细胞对BDG的摄取具有饱和性。胆红素、磺溴酞钠和胆红素单葡萄糖醛酸酯可抑制这种摄取，但牛磺胆酸盐无此作用。除胆碱外，用其他阳离子替代钠离子时，摄取不受影响。只有用胆碱替代钠离子时，才观察到摄取显著下降。用硝酸盐替代氯化物时，BDG摄取减少，但用硫酸盐替代则无变化。代谢抑制剂对BDG摄取无明显影响。因此，胆汁色素在肝细胞膜上共享一种不依赖钠离子且依赖电位的电生性共同转运体。高浓度白蛋白会干扰BDG摄取。
