Hotta N, Kakuta H, Fukasawa H, Kimura M, Koh N, Matsumae H, Fujimaki M, Sakamoto N
Third Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Horm Metab Res. 1988 Jul;20(7):387-90. doi: 10.1055/s-2007-1010843.
Myo-inositol uptake by erythrocytes from humans, rabbits and rats was studied with an isotope technique. In human erythrocytes, the inhibitory effect on myo-inositol uptake was stronger with glucose than with ouabain. However, an aldose reductase inhibitor (ONO-2235, 100 microM) or insulin (200 microU/ml) failed to correct the decrease in myo-inositol uptake in packed RBC, produced by either 10 mM glucose or 2mM ouabain. Ten mM ouabain had an inhibitory effect on myo-inositol uptake in all species, but an inhibitory effect was not observed with 20 mM glucose in rabbit erythrocytes. The results suggest that myo-inositol uptake by erythrocytes may be dependent on the active transport system via sodium-ATPase and that erythrocytes may not be a suitable model to monitor the possible effect of an aldose reductase inhibitor on myo-inositol concentrations in other tissues concerned with diabetic complications.
采用同位素技术研究了人、兔和大鼠红细胞对肌醇的摄取。在人红细胞中，葡萄糖对肌醇摄取的抑制作用强于哇巴因。然而，醛糖还原酶抑制剂（ONO - 2235，100微摩尔）或胰岛素（200微单位/毫升）未能纠正由10毫摩尔葡萄糖或2毫摩尔哇巴因引起的压积红细胞中肌醇摄取的减少。10毫摩尔哇巴因对所有物种的红细胞肌醇摄取均有抑制作用，但20毫摩尔葡萄糖对兔红细胞的肌醇摄取未观察到抑制作用。结果表明，红细胞对肌醇的摄取可能依赖于通过钠 - ATP酶的主动转运系统，并且红细胞可能不是监测醛糖还原酶抑制剂对与糖尿病并发症相关的其他组织中肌醇浓度可能产生影响的合适模型。
