Li S H, McNeill J H
Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, Canada.
Mol Cell Biochem. 2001 Jan;217(1-2):121-9. doi: 10.1023/a:1007224828753.
The effect of vanadium treatment on insulin-stimulated glucose transporter type 4 (GLUT4) translocation was studied in cardiac tissue of streptozotocin (STZ)-induced diabetic rats by determining the subcellular distribution of GLUT4. Four groups of rats were examined: control and diabetic, with or without bis(maltolato)oxovanadium(IV) (BMOV, an organic form of vanadium) treatment for 8 weeks. The effect of vanadium on insulin-induced GLUT4 translocation was studied at 5 min as the early insulin response and at 15 min after insulin injection as the maximal insulin response. At 5 min after insulin injection, plasma membrane GLUT4 level in the diabetic-treated group was not different from the control groups and was significantly higher than that of the insulin-stimulated diabetic group, indicating an enhancement of insulin response on GLUT4 translocation brought about by vanadium treatment. In contrast to that at 5 min after insulin injection, no significant difference in the plasma membrane GLUT4 level was observed between the diabetic and the diabetic-treated groups at 15 min after insulin injection. GLUT4 mobilization from the intracellular pool in response to insulin was also investigated at 15 min after insulin injection. Basal intracellular GLUT4 content was significantly higher in the diabetic-treated group when compared to the diabetic group under the same condition. However, the increased basal intracellular GLUT4 in the diabetic-treated group did not result in more insulin-mediated GLUT4 translocation at 15 min after insulin injection. In conclusion, the finding that plasma membrane GLUT4 in the diabetic-treated group is significantly higher than that of the diabetic group at 5 min but not at 15 min post-insulin injection indicates that vanadium treatment enhances insulin-mediated GLUT4 translocation in cardiac tissue by enhancing its early response.
通过测定葡萄糖转运蛋白4（GLUT4）的亚细胞分布，研究了钒处理对链脲佐菌素（STZ）诱导的糖尿病大鼠心脏组织中胰岛素刺激的GLUT4转位的影响。研究了四组大鼠：对照组和糖尿病组，分别接受或不接受双（麦芽酚）氧钒（IV）（BMOV，一种有机形式的钒）处理8周。在胰岛素注射后5分钟作为早期胰岛素反应以及在胰岛素注射后15分钟作为最大胰岛素反应，研究了钒对胰岛素诱导的GLUT4转位的影响。胰岛素注射后5分钟，糖尿病治疗组的质膜GLUT4水平与对照组无差异，且显著高于胰岛素刺激的糖尿病组，表明钒处理增强了胰岛素对GLUT4转位的反应。与胰岛素注射后5分钟的情况相反，胰岛素注射后15分钟，糖尿病组和糖尿病治疗组之间的质膜GLUT4水平没有显著差异。在胰岛素注射后15分钟也研究了GLUT4从细胞内池对胰岛素的动员情况。在相同条件下，糖尿病治疗组的基础细胞内GLUT4含量显著高于糖尿病组。然而，糖尿病治疗组基础细胞内GLUT4的增加并没有导致胰岛素注射后15分钟更多的胰岛素介导的GLUT4转位。总之，糖尿病治疗组在胰岛素注射后5分钟质膜GLUT4显著高于糖尿病组，但在15分钟时并非如此，这一发现表明钒处理通过增强早期反应增强了心脏组织中胰岛素介导的GLUT4转位。
