Hamada Taku, Arias Edward B, Cartee Gregory D
Muscle Biology Laboratory, Division of Kinesiology, University of Michigan, Ann Arbor, MI 48109-2214, USA.
J Appl Physiol (1985). 2006 Nov;101(5):1368-76. doi: 10.1152/japplphysiol.00416.2006. Epub 2006 Jun 29.
The primary purpose of this study was to determine the effect of prior exercise on insulin-stimulated glucose uptake with physiological insulin in isolated muscles of mice. Male C57BL/6 mice completed a 60-min treadmill exercise protocol or were sedentary. Paired epitrochlearis, soleus, and extensor digitorum longus (EDL) muscles were incubated with [3H]-2-deoxyglucose without or with insulin (60 microU/ml) to measure glucose uptake. Insulin-stimulated glucose uptake for paired muscles was calculated by subtracting glucose uptake without insulin from glucose uptake with insulin. Muscles from other mice were assessed for glycogen and AMPK Thr172 phosphorylation. Exercised vs. sedentary mice had decreased glycogen in epitrochlearis (48%, P < 0.001), soleus (51%, P < 0.001), and EDL (41%, P < 0.01) and increased AMPK Thr172 phosphorylation (P < 0.05) in epitrochlearis (1.7-fold), soleus (2.0-fold), and EDL (1.4-fold). Insulin-independent glucose uptake was increased 30 min postexercise vs. sedentary in the epitrochlearis (1.2-fold, P < 0.001), soleus (1.4-fold, P < 0.05), and EDL (1.3-fold, P < 0.01). Insulin-stimulated glucose uptake was increased (P < 0.05) approximately 85 min after exercise in the epitrochlearis (sedentary: 0.266 +/- 0.045 micromol x g(-1) x 15 min(-1); exercised: 0.414 +/- 0.051) and soleus (sedentary: 0.102 +/- 0.049; exercised: 0.347 +/- 0.098) but not in the EDL. Akt Ser473 and Akt Thr308 phosphorylation for insulin-stimulated muscles did not differ in exercised vs. sedentary. These results demonstrate enhanced submaximal insulin-stimulated glucose uptake in the epitrochlearis and soleus of mice 85 min postexercise and suggest that it will be feasible to probe the mechanism of enhanced postexercise insulin sensitivity by using genetically modified mice.
本研究的主要目的是确定预先运动对小鼠离体肌肉中生理胰岛素刺激的葡萄糖摄取的影响。雄性C57BL/6小鼠完成60分钟的跑步机运动方案或保持久坐。将配对的肱三头肌、比目鱼肌和趾长伸肌（EDL）肌肉与[3H]-2-脱氧葡萄糖一起孵育，分别在无胰岛素或有胰岛素（60微单位/毫升）的情况下测量葡萄糖摄取。通过用有胰岛素时的葡萄糖摄取量减去无胰岛素时的葡萄糖摄取量来计算配对肌肉的胰岛素刺激的葡萄糖摄取量。对来自其他小鼠的肌肉进行糖原和AMPK Thr172磷酸化评估。运动小鼠与久坐小鼠相比，肱三头肌中的糖原减少（48%，P<0.001），比目鱼肌中的糖原减少（51%，P<0.001），EDL中的糖原减少（41%，P<0.01），并且肱三头肌（1.7倍）、比目鱼肌（2.0倍）和EDL（1.4倍）中的AMPK Thr172磷酸化增加（P<0.05）。运动后30分钟，肱三头肌（1.2倍，P<0.001）、比目鱼肌（1.4倍，P<0.05）和EDL（1.3倍，P<0.01）中与胰岛素无关的葡萄糖摄取相对于久坐小鼠增加。运动后约85分钟，肱三头肌（久坐：0.266±0.045微摩尔×克-1×15分钟-1；运动：0.414±0.051）和比目鱼肌（久坐：0.102±0.049；运动：0.347±0.098）中胰岛素刺激的葡萄糖摄取增加（P<0.05），但EDL中未增加。运动小鼠与久坐小鼠相比，胰岛素刺激的肌肉中Akt Ser473和Akt Thr308磷酸化没有差异。这些结果表明，运动后85分钟小鼠肱三头肌和比目鱼肌中次最大胰岛素刺激的葡萄糖摄取增强，并且表明通过使用基因改造小鼠来探究运动后胰岛素敏感性增强的机制将是可行的。
