Muscle alpha-aminoisobutyric acid transport after exercise: enhanced stimulation by insulin.
Muscle alpha-aminoisobutyric acid transport after exercise: enhanced stimulation by insulin.
复制标题
运动后肌肉α-氨基异丁酸转运：胰岛素增强刺激。
DOI：
10.1152/ajpendo.1985.248.5.e546
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Ruderman,NB
中科院分区：
文献类型：
--
作者：
Zorzano,A;Balon,TW;Garetto,LP;Goodman,MN;Ruderman,NB
运动后，胰岛素刺激大鼠骨骼肌中葡萄糖转运和糖原合成的能力显著增强（25）。本研究旨在确定先前的运动是否增加了胰岛素对其他过程的刺激，如果是这样，这是否可以归因于胰岛素与其受体结合的增加。为此，大鼠在跑步机上以中等强度跑45分钟，然后使用分离的灌注后腿制备物评估肌肉对α-氨基异丁酸（AIB）的摄取。运动停止后约30分钟，在比目鱼肌和腓肠肌的红色部分中，胰岛素刺激的AIB摄取的敏感性和反应性均显著增强。如之前所示，对于葡萄糖转运和糖原合成，仅在腓肠肌的白色部分观察到很小的影响，与其他肌肉不同，该部分在跑步过程中没有耗尽糖原。胰岛素刺激的葡萄糖利用率也提高了在孵育的比目鱼肌锻炼大鼠，但是，胰岛素结合比目鱼肌没有改变。这些研究表明，运动后骨骼肌中胰岛素刺激葡萄糖转运和糖原合成以外的过程的能力增强，这不是由于胰岛素结合的改变。运动后胰岛素刺激的AIB摄取和葡萄糖代谢的变化与失神经和固定肌肉中发现的变化相反，并且在这两种情况下胰岛素结合没有改变。这表明一个共同的因素调节运动后胰岛素效应的增加和废用性胰岛素抵抗。
After exercise the ability of insulin to stimulate glucose transport and glycogen synthesis in rat skeletal muscle is markedly enhanced (25). The present study was designed to determine whether prior exercise augments the stimulation of other processes by insulin and, if so, whether this can be attributed to an increase in insulin binding to its receptor. Toward this end rats were run on a treadmill for 45 min at moderate intensity and the uptake of alpha-aminoisobutyric acid (AIB) by muscle was then assessed using the isolated perfused hindquarter preparation. Approximately 30 min after the cessation of exercise, both the sensitivity and responsiveness of insulin-stimulated AIB uptake were significantly enhanced in the soleus and the red portion of the gastrocnemius. As previously shown for glucose transport and glycogen synthesis, only small effects were observed in the white portion of the gastrocnemius, which unlike the other muscles was not depleted of glycogen during the run. Insulin-stimulated glucose utilization was also enhanced in the incubated soleus muscle of exercised rats; however, insulin binding to the soleus was not altered. These studies indicate that the ability of insulin to stimulate processes other than glucose transport and glycogen synthesis is enhanced in skeletal muscle after exercise and that this is not due to an alteration in insulin binding. The changes in insulin-stimulated AIB uptake and glucose metabolism after exercise are the reverse of those found in denervated and immobilized muscle and in both situations insulin binding is not altered. This suggests that a common factor(s) modulates the increase in insulin effect after exercise and the insulin resistance of disuse.