Uemura Etsuro, Greenlee Heather West
Department of Biomedical Sciences, Iowa State University, Ames, IA 50011, USA.
Exp Neurol. 2006 Mar;198(1):48-53. doi: 10.1016/j.expneurol.2005.10.035. Epub 2005 Dec 9.
Neurons have been classically considered insulin-insensitive cells. In this in vitro study, the effect of insulin on neuronal glucose uptake was studied by assaying glucose uptake, translocation of glucose transporter isoform GLUT3, and fusion of GLUT3 vesicles with the plasma membrane. Insulin (50 nM) promoted translocation of GLUT3 to the plasma membrane. However, insulin neither promoted fusion of GLUT3 with the plasma membrane nor increased neuronal glucose uptake. In cells pre-exposed to insulin, depolarization with 40 mM KCl markedly increased fusion of GLUT3 with plasma membrane and neuronal uptake of glucose. Based on these data, we propose that insulin regulates neuronal glucose uptake by promoting translocation of GLUT3 to the plasma membrane, and that insulin enables neurons to respond to demand for energy induced by increased neuronal activity.
神经元传统上被认为是对胰岛素不敏感的细胞。在这项体外研究中，通过检测葡萄糖摄取、葡萄糖转运蛋白异构体GLUT3的转位以及GLUT3囊泡与质膜的融合，研究了胰岛素对神经元葡萄糖摄取的影响。胰岛素（50 nM）促进了GLUT3向质膜的转位。然而，胰岛素既不促进GLUT3与质膜的融合，也不增加神经元葡萄糖摄取。在预先暴露于胰岛素的细胞中，用40 mM KCl进行去极化显著增加了GLUT3与质膜的融合以及神经元对葡萄糖的摄取。基于这些数据，我们提出胰岛素通过促进GLUT3向质膜的转位来调节神经元葡萄糖摄取，并且胰岛素使神经元能够响应神经元活动增加所诱导的能量需求。
