O'Gorman D J, Karlsson H K R, McQuaid S, Yousif O, Rahman Y, Gasparro D, Glund S, Chibalin A V, Zierath J R, Nolan J J
Metabolic Research Unit, St James's Hospital, Trinity College, Dublin, Ireland.
Diabetologia. 2006 Dec;49(12):2983-92. doi: 10.1007/s00125-006-0457-3. Epub 2006 Sep 26.
AIMS/HYPOTHESIS: Exercise enhances insulin-stimulated glucose transport in skeletal muscle through changes in signal transduction and gene expression. The aim of this study was to assess the impact of acute and short-term exercise training on whole-body insulin-mediated glucose disposal and signal transduction along the canonical insulin signalling cascade.
A euglycaemic-hyperinsulinaemic clamp, with vastus lateralis skeletal muscle biopsies, was performed at baseline and 16 h after an acute bout of exercise and short-term exercise training (7 days) in obese non-diabetic (n=7) and obese type 2 diabetic (n=8) subjects.
Insulin-mediated glucose disposal was unchanged following acute exercise in both groups. Short-term exercise training increased insulin-mediated glucose disposal in obese type 2 diabetic (p<0.05), but not in obese non-diabetic subjects. Insulin activation of (1) IRS1, (2) IRS2, (3) phosphotyrosine-associated phosphatidylinositol-3 kinase activity and (4) the substrate of phosphorylated Akt, AS160, a functional Rab GTPase activating protein important for GLUT4 (now known as solute carrier family 2 [facilitated glucose transporter], member 4 [SLC2A4]) translocation, was unchanged after acute or chronic exercise in either group. GLUT4 protein content was increased in obese type 2 diabetic subjects (p<0.05), but not in obese non-diabetic subjects following chronic exercise.
CONCLUSIONS/INTERPRETATION: Exercise training increased whole-body insulin-mediated glucose disposal in obese type 2 diabetic patients. These changes were independent of functional alterations in the insulin-signalling cascade and related to increased GLUT4 protein content.
目的/假设：运动通过信号转导和基因表达的变化增强骨骼肌中胰岛素刺激的葡萄糖转运。本研究的目的是评估急性和短期运动训练对全身胰岛素介导的葡萄糖处置以及经典胰岛素信号级联反应中信号转导的影响。
在肥胖非糖尿病患者（n = 7）和肥胖2型糖尿病患者（n = 8）中，于基线、急性运动 bout 后16小时以及短期运动训练（7天）后，进行了伴有股外侧肌骨骼肌活检的正常血糖 - 高胰岛素钳夹试验。
两组急性运动后胰岛素介导的葡萄糖处置均未改变。短期运动训练增加了肥胖2型糖尿病患者胰岛素介导的葡萄糖处置（p<0.05），但肥胖非糖尿病患者未增加。两组在急性或慢性运动后，胰岛素对（1）IRS1、（2）IRS2、（3）磷酸酪氨酸相关磷脂酰肌醇 - 3激酶活性以及（4）磷酸化Akt的底物AS160（一种对GLUT4[现称为溶质载体家族2（促进性葡萄糖转运蛋白），成员4（SLC2A4）]易位重要的功能性Rab GTP酶激活蛋白）的激活均未改变。慢性运动后，肥胖2型糖尿病患者的GLUT4蛋白含量增加（p<0.05），但肥胖非糖尿病患者未增加。
结论/解读：运动训练增加了肥胖2型糖尿病患者全身胰岛素介导的葡萄糖处置。这些变化与胰岛素信号级联反应中的功能改变无关，而与GLUT4蛋白含量增加有关。
