Wang C, Hsieh C H, Wu W G
Institute of Molecular Biology, Academia Sinica, Nankang, Taipei, Taiwan, ROC.
Biochem Biophys Res Commun. 1991 Apr 15;176(1):201-6. doi: 10.1016/0006-291x(91)90909-q.
Phenylarsine oxide (PAO) is known to block insulin-stimulated glucose transport activity in 3T3 L1 adipocytes at a post-receptor step. Herein, we demonstrate that, at right concentration, PAO also inhibits insulin activation of glucose uptake in rat soleus muscles but does not affect basal level of uptake. In control experiments, insulin stimulation of 2-deoxy-D-glucose uptake is about 400% of that of the control level. After PAO treatment, the stimulation reduces to 150% of the control. Since the intracellular level of ATP remains unchanged after PAO treatment, when measured by phosphorus-31 nmr spectroscopy, this inhibition is not due to depletion of ATP pool size. Moreover, PAO does not affect autophosphorylation of the insulin receptors purified from rat soleus muscles, implying that the PAO blockage of insulin-dependent glucose uptake in soleus muscles also may be post-receptor.
已知氧化苯胂(PAO)在受体后步骤阻断3T3 L1脂肪细胞中胰岛素刺激的葡萄糖转运活性。在此,我们证明,在合适的浓度下,PAO也抑制大鼠比目鱼肌中胰岛素激活的葡萄糖摄取,但不影响基础摄取水平。在对照实验中,胰岛素刺激的2-脱氧-D-葡萄糖摄取约为对照水平的400%。PAO处理后,刺激降低至对照的150%。当通过磷-31核磁共振光谱法测量时,由于PAO处理后细胞内ATP水平保持不变,这种抑制不是由于ATP池大小的耗竭。此外,PAO不影响从大鼠比目鱼肌纯化的胰岛素受体的自身磷酸化,这意味着PAO对胰岛素依赖的比目鱼肌葡萄糖摄取的阻断也可能发生在受体后。