Olefsky J M
Biochem J. 1978 Apr 15;172(1):137-45. doi: 10.1042/bj1720137.
Isolated rat adipocytes were used to assess the mechanisms of the ability of insulin to accelerate glucose transport. Glucose transport was determined by measuring the initial rates of 2-deoxyglucose uptake, and at 24 degrees C insulin increased the Vmax. of transport from 7.3 +/- 1 to 23.1 +/- 2 nmol/min per 10(6) cells, but the Km value remained unchanged (2.5, cf. 2.4 mM). When the Vmax. of basal and insulin-stimulated transport was measured as a function of temperature (15-37 degrees C), parallel Arrhenius plots were obtained yielding equal activation energies of approx. 59kJ/mol. Since both processes have equal activation energies the data indicate that insulin increases Vmax. by increasing the number of available carriers rather than enhancing intrinsic activity of already functioning carriers. Since the ability of insulin to activate glucose transport did not decrease with temperature (whereas plasma-membrane fluidity declines), it is suggested that lateral diffusion of insulin receptors within the plasma-membrane bilayer is not a rat-determining step in insulin action.
分离的大鼠脂肪细胞被用于评估胰岛素加速葡萄糖转运能力的机制。通过测量2-脱氧葡萄糖摄取的初始速率来测定葡萄糖转运，在24℃时胰岛素使转运的Vmax从每10(6)个细胞7.3±1增加到23.1±2nmol/分钟，但Km值保持不变(2.5，对比2.4mM)。当测量基础和胰岛素刺激的转运的Vmax作为温度(15 - 37℃)的函数时，得到平行的阿累尼乌斯图，产生约59kJ/mol的相等活化能。由于这两个过程具有相等的活化能，数据表明胰岛素通过增加可用载体的数量而不是增强已发挥功能的载体的内在活性来增加Vmax。由于胰岛素激活葡萄糖转运的能力不会随温度降低(而质膜流动性下降)，提示胰岛素受体在质膜双层内的侧向扩散不是胰岛素作用的限速步骤。
