Asada T, Takakura S, Ogawa T, Iwai M, Kobayashi M
Molecular Biological Research Laboratories, Fujisawa Pharmaceutical, Osaka, Japan.
Neurosci Lett. 1998 Aug 14;252(2):111-4. doi: 10.1016/s0304-3940(98)00560-6.
The localization and the expression level of glucose transporter 5 (GLUT 5), detected by immunohistochemical and Western blot analyses, and motor nerve conduction velocity (MNCV) in normal and streptozotocin (STZ)-induced diabetic rats were compared. The effects of insulin and recombinant human insulin-like growth factor-I (rhIGF-I) were also investigated. GLUT 5 was localized in Schwann cells and axons. GLUT 5 was overexpressed in both sites 5 weeks after STZ injection and MNCV was decreased significantly in STZ-induced diabetic rats as compared with normal rats. These deviations returned to normal rat level after 2 weeks medication with insulin or rhIGF-I, started 3 weeks after STZ injection. These results suggest that overexpression of GLUT 5 may be a trigger for diabetic neuropathy.
通过免疫组织化学和蛋白质印迹分析检测正常大鼠和链脲佐菌素（STZ）诱导的糖尿病大鼠中葡萄糖转运蛋白5（GLUT 5）的定位和表达水平，并比较运动神经传导速度（MNCV）。还研究了胰岛素和重组人胰岛素样生长因子-I（rhIGF-I）的作用。GLUT 5定位于雪旺细胞和轴突。STZ注射后5周，GLUT 5在这两个部位均过度表达，与正常大鼠相比，STZ诱导的糖尿病大鼠的MNCV显著降低。在STZ注射3周后开始用胰岛素或rhIGF-I治疗2周后，这些偏差恢复到正常大鼠水平。这些结果表明，GLUT 5的过度表达可能是糖尿病神经病变的触发因素。
