Venkatesan N, Davidson M B
Life Sci. 1983 Jan 31;32(5):467-74. doi: 10.1016/0024-3205(83)90139-x.
The possibility of Ca++ acting as second messenger for insulin in rat liver was investigated using the net stimulation of 14C-glucose incorporation into glycogen by isolated hepatocytes as an index of insulin action. An insulin effect could be partially sustained in the virtual absence of Ca++ and Mg++ and a maximal insulin effect could be observed in the presence of either Ca++ or Mg++, suggesting that extracellular Ca++ is not required for insulin action. Inhibiting the activity of calmodulin, an intracellular mediator of Ca++ action, with trifluoperazine had little effect on insulin action. The efflux of 45Ca from prelabeled hepatocytes was not altered by the presence of insulin arguing against insulin-induced changes in Ca++ fluxes. Collectively, these results do not support the role of Ca++ as second messenger for insulin action in liver.
利用分离的肝细胞将14C-葡萄糖掺入糖原的净刺激作为胰岛素作用的指标，研究了Ca++作为大鼠肝脏中胰岛素第二信使的可能性。在几乎没有Ca++和Mg++的情况下，胰岛素效应仍可部分维持，在存在Ca++或Mg++的情况下可观察到最大胰岛素效应，这表明胰岛素作用不需要细胞外Ca++。用三氟拉嗪抑制钙调蛋白（Ca++作用的细胞内介质）的活性对胰岛素作用影响很小。预先标记的肝细胞中45Ca的流出不受胰岛素存在的影响，这与胰岛素诱导的Ca++通量变化相矛盾。总体而言，这些结果不支持Ca++作为肝脏中胰岛素作用第二信使的作用。
