Resh M D
Biochemistry. 1983 Jun 7;22(12):2781-4. doi: 10.1021/bi00281a001.
The time course of insulin activation of sodium and potassium ion activated adenosinetriphosphatase [(Na+,K+)ATPase] was studied in the rat adipocyte and was compared to activation of the glucose transporter. Under conditions in which the binding of insulin to its cell surface receptor was not rate limiting, a distinct time lag was apparent between insulin addition and stimulation of transport activity. At 37 degrees C, 40-50 s elapsed before an increase in Rb+ uptake [a measure of (Na+,K+)ATPase transport activity] or 2-deoxyglucose uptake could be observed. This lag time increased in an identical manner for both transport processes as the temperature was lowered to 23 degrees C. Addition of the insulinomimetic agent hydrogen peroxide also produced a lag time similar to that for insulin before activation of Rb+ and 2-deoxyglucose uptakes was detected. These data provide the first evidence of a discrete time lag involved during stimulation of the adipocyte (Na+,K+)ATPase. A model for the molecular mechanism of insulin activation of (Na+,K+)ATPase is presented that incorporates these results into the hypothesis of insulin mediated "translocation" of glucose transporters to the plasma membrane.
在大鼠脂肪细胞中研究了胰岛素激活钠钾离子激活的三磷酸腺苷酶[(Na +,K +)ATP酶]的时间进程,并与葡萄糖转运体的激活进行了比较。在胰岛素与其细胞表面受体的结合不是限速步骤的条件下,添加胰岛素与刺激转运活性之间存在明显的时间滞后。在37℃时,在观察到铷摄取增加[(Na +,K +)ATP酶转运活性的一种测量方法]或2-脱氧葡萄糖摄取增加之前经过了40 - 50秒。随着温度降低到23℃,两种转运过程的滞后时间以相同方式增加。添加胰岛素模拟剂过氧化氢在检测到铷和2-脱氧葡萄糖摄取激活之前也产生了与胰岛素相似的滞后时间。这些数据首次证明了脂肪细胞(Na +,K +)ATP酶刺激过程中存在离散的时间滞后。提出了一个胰岛素激活(Na +,K +)ATP酶分子机制的模型,该模型将这些结果纳入胰岛素介导的葡萄糖转运体“易位”到质膜的假说中。