Passive stretching produces Akt- and MAPK-dependent augmentations of GLUT4 translocation and glucose uptake in skeletal muscles of mice
Passive stretching produces Akt- and MAPK-dependent augmentations of GLUT4 translocation and glucose uptake in skeletal muscles of mice
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DOI：
10.1007/s00424-005-1512-5
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发表时间：
2006-03-01
影响因子：
4.5
通讯作者：
Nakayama, K
中科院分区：
文献类型：
--
作者：
Ito, Y;Obara, K;Nakayama, K
肌肉收缩伴随着细胞和组织的被动拉伸或变形。本研究旨在阐明急性被动拉伸是否引起小鼠骨骼肌葡萄糖转运蛋白4（GLUT 4）移位和葡萄糖摄取。被动牵张主要诱导GLUT 4从胞内膜富集组分（PF 5）向质膜富集组分（F2）移位，促进后肢肌肉葡萄糖摄取;而模拟体内体育锻炼的电刺激和胰岛素各自诱导GLUT 4从富含细胞内膜的级分（PF 5）移位到富含质膜的级分（F2），一个富含横小管（PF 3），沿着随后的葡萄糖摄取。机械牵张可增加Akt和p38丝裂原活化蛋白激酶（p38 MAPK）的磷酸化水平，但对AMP活化蛋白激酶（AMPK）活性无明显影响。电刺激不仅增强AMPK的活性，而且增强Akt和p38 MAPK的磷酸化。我们的研究结果表明，被动拉伸产生的GLUT 4主要是从富含细胞内膜的部分，富含质膜的易位，葡萄糖的摄取可能是Akt和p38 MAPK依赖的，但AMPK的独立方式。
Muscle contraction is accompanied by passive stretching or deformation of cells and tissues. The present study aims to clarify whether or not acute passive stretching evokes glucose transporter 4 (GLUT4) translocation and glucose uptake in skeletal muscles of mice. Passive stretching mainly induced GLUT4 translocation from an intracellular membrane-rich fraction (PF5) to a plasma membrane-rich fraction (F2) and accelerated glucose uptake in hindlimb muscles; whereas electrical stimulation, which mimics physical exercise in vivo, and insulin, each induced GLUT4 translocation from an intracellular membrane-rich fraction (PF5) to a fraction rich in plasma membrane (F2), and to one rich in transverse tubules (PF3), along with subsequent glucose uptake. Mechanical stretching increased phosphorylation of Akt and p38 mitogen-activated protein kinase (p38 MAPK), but it had no apparent effect on the activity of AMP-activated protein kinase (AMPK). Electrical stimulation augmented the activity of not only AMPK but also phosphorylation of Akt and p38 MAPK. Our results suggest that passive stretching produces translocation of GLUT4 mainly from the fraction rich in intracellular membrane to that rich in plasma membrane, and that the glucose uptake could be Akt- and p38 MAPK-dependent, but AMPK-independent manners.