Satoh S, Nishimura H, Clark A E, Kozka I J, Vannucci S J, Simpson I A, Quon M J, Cushman S W, Holman G D
Experimental Diabetes, Metabolism, and Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
J Biol Chem. 1993 Aug 25;268(24):17820-9.
The subcellular trafficking of tracer-tagged GLUT4 between the plasma membranes and low-density microsomes of rat adipose cells has been studied. Cell-surface GLUT4 have been initially tracer-tagged in the insulin-stimulated state with the [3H]bismanose photolabel 2-N-4-(1-azi-2,2,2-trifluoroethyl)benzoyl-1,3-bis-(D-mannos- 4-yloxy)-2- propylamine. The half-time for internalization of tracer-tagged GLUT4 when insulin is removed by collagenase treatment is similar to that observed for the decrease in immunodetectable GLUT4 in the plasma membranes and the decrease in glucose transport activity in the intact cells. In contrast, internalization of tracer-tagged GLUT4 also occurs when cells are maintained in the continuous presence of insulin even though the plasma membrane level of immunodetectable GLUT4 and glucose transport activity in the intact cells are unaltered. These data show, for the first time, that insulin has little, if any, effect on the rate constant for GLUT4 endocytosis, but instead, primarily increases the rate constant for exocytosis. Tracer-tagged GLUT4 that is returned to the low-density microsomes can be restimulated with fresh insulin to recycle to the plasma membranes and to a steady-state distribution level that is the same as that observed in cells that are maintained in the continuous presence of insulin. These data suggest that the cells' entire complement of GLUT4 is involved in the recycling process. Following insulin stimulation of adipose cells initially in the basal state, the increase in immunodetectable GLUT4 in the plasma membranes precedes the increase in accessibility of GLUT4 to exofacial 2-N-4-(1-azi-2,2,2-trifluoroethyl)benzoyl-1,3-bis(D-mannos-4 -yloxy)-2- propylamine photolabeling, and this in turn precedes the increase in cellular glucose transport activity. Such time course data suggest that there may be plasma membrane intermediate states in the GLUT4 trafficking pathway. The kinetic properties of GLUT4 translocation and its recycling have been interpreted in terms of a subcellular trafficking model that identifies exocytosis, possibly involving-hypothetical "docking" and "fusion" steps, as the critical site of hormone action.
对示踪剂标记的GLUT4在大鼠脂肪细胞质膜和低密度微粒体之间的亚细胞转运进行了研究。细胞表面的GLUT4最初在胰岛素刺激状态下用[3H]双甘露糖光标记物2-N-4-(1-叠氮基-2,2,2-三氟乙基)苯甲酰基-1,3-双-(D-甘露糖-4-氧基)-2-丙胺进行标记。当通过胶原酶处理去除胰岛素后,示踪剂标记的GLUT4内化的半衰期与质膜中免疫可检测的GLUT4减少以及完整细胞中葡萄糖转运活性降低所观察到的半衰期相似。相比之下,即使完整细胞中免疫可检测的GLUT4质膜水平和葡萄糖转运活性未改变,当细胞在胰岛素持续存在的情况下维持时,示踪剂标记的GLUT4也会发生内化。这些数据首次表明,胰岛素对GLUT4内吞作用的速率常数几乎没有影响(如果有影响的话),但相反,主要增加了胞吐作用的速率常数。回到低密度微粒体的示踪剂标记的GLUT4可以用新鲜胰岛素重新刺激,以循环回到质膜并达到与在胰岛素持续存在的情况下维持的细胞中观察到的相同的稳态分布水平。这些数据表明细胞中GLUT4的整个补充都参与了循环过程。在最初处于基础状态的脂肪细胞受到胰岛素刺激后,质膜中免疫可检测的GLUT4增加先于GLUT4对外表面2-N-4-(1-叠氮基-2,2,2-三氟乙基)苯甲酰基-1,3-双-(D-甘露糖-4-氧基)-2-丙胺光标记的可及性增加,而这又先于细胞葡萄糖转运活性的增加。这样的时间进程数据表明,在GLUT4转运途径中可能存在质膜中间状态。GLUT4易位及其循环的动力学特性已根据亚细胞转运模型进行了解释,该模型将胞吐作用(可能涉及假设的“对接”和“融合”步骤)确定为激素作用的关键位点。