Liu D, Chen C C, Chai S P, Ho L T, Fong J C
Institute of Biochemistry, National Yang-Ming University, Taipei, Taiwan, Republic of China.
Biochem Mol Biol Int. 1998 Nov;46(4):681-8. doi: 10.1080/15216549800204212.
The effect of arachidonic acid (AA) on insulin-stimulated glucose transport by 3T3-L1 adipocytes was examined in the presence of cycloheximide. We found that AA acted synergistically with cycloheximide to suppress insulin-stimulated glucose transport, although it alone was without effect. Similar phenomena were observed while protein synthesis inhibitors other than cycloheximide were employed. Immunoblot analysis indicated that the increase in plasma membranes of the insulin-regulated glucose transporter (GLUT4) in response to insulin was decreased in cells pretreated with cycloheximide for a prolonged time, while total amount of GLUT4 was not altered. Simultaneous presence of AA with cycloheximide had no further effect on the amount of GLUT4 in either total or plasma membranes. Thus the present study suggests that AA in the presence of a protein synthesis inhibitor seems to decrease the intrinsic activity of GLUT4.
在存在放线菌酮的情况下，研究了花生四烯酸（AA）对3T3-L1脂肪细胞胰岛素刺激的葡萄糖转运的影响。我们发现，AA与放线菌酮协同作用以抑制胰岛素刺激的葡萄糖转运，尽管其单独作用时没有效果。当使用除放线菌酮以外的蛋白质合成抑制剂时，也观察到了类似现象。免疫印迹分析表明，长时间用放线菌酮预处理的细胞中，胰岛素调节的葡萄糖转运蛋白（GLUT4）质膜上因胰岛素产生的增加减少了，而GLUT4的总量没有改变。AA与放线菌酮同时存在对总膜或质膜中GLUT4的量没有进一步影响。因此，本研究表明，在存在蛋白质合成抑制剂的情况下，AA似乎会降低GLUT4的内在活性。
