Stöckli Jacqueline, Fazakerley Daniel J, Coster Adelle C F, Holman Geoffrey D, James David E
Commun Integr Biol. 2010 May;3(3):260-2. doi: 10.4161/cib.3.3.11457.
Insulin triggers glucose uptake into muscle and adipose tissue by stimulating the translocation of the glucose transporter glut4 from intracellular vesicles to the plasma membrane (pm). insulin leads to a rapid increase in glut4 at the pm from approximately 5% to 40-50%. this effect is time and dose-dependent, reaching a new steady state after 30 min of insulin stimulation. previous kinetic analyses in adipocytes has revealed that this is regulated by two mechanisms-increasing the amount of glut4 in the endosomal recycling system and increasing the exocytosis rate constant. fazakerley et al.1 focuses on GLUT4 kinetics in the L6 skeletal muscle cell line. Despite displaying a similar redistribution of GLUT4 to the cell surface with insulin to that seen in adipocytes, the mechanism for this effect in L6 cells was completely different. Insulin had a modest effect to increase the amount of GLUT4 in the recycling system with the dominant effect being on reduction of the endocytosis rate constant. Similar findings were observed with AMPK agonists. These studies indicate that different cell types are capable of achieving the same cell biological endpoint but using completely distinct mechanisms.
胰岛素通过刺激葡萄糖转运蛋白4（glut4）从细胞内囊泡转运至质膜（pm），从而促使葡萄糖摄取进入肌肉和脂肪组织。胰岛素可使质膜上的glut4迅速增加，从约5%升至40 - 50%。这种效应具有时间和剂量依赖性，在胰岛素刺激30分钟后达到新的稳态。先前对脂肪细胞的动力学分析表明，这一过程受两种机制调控——增加内体循环系统中glut4的量以及提高胞吐速率常数。法扎克利等人[1]聚焦于L6骨骼肌细胞系中的GLUT4动力学。尽管L6细胞中GLUT4向细胞表面的重新分布与脂肪细胞中胰岛素作用下的情况相似，但其作用机制却完全不同。胰岛素对增加循环系统中GLUT4的量作用不大，主要作用是降低内吞速率常数。用AMPK激动剂也观察到了类似的结果。这些研究表明，不同细胞类型能够通过完全不同的机制实现相同的细胞生物学终点。
