CONTRACTILE ACTIVITY RESTORES INSULIN RESPONSIVENESS IN SKELETAL-MUSCLE OF OBESE ZUCKER RATS
CONTRACTILE ACTIVITY RESTORES INSULIN RESPONSIVENESS IN SKELETAL-MUSCLE OF OBESE ZUCKER RATS
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DOI：
10.1042/bj2890423
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发表时间：
1993-01-15
影响因子：
4.1
通讯作者：
DOHM, GL
中科院分区：
文献类型：
--
作者：
DOLAN, PL;TAPSCOTT, EB;DOHM, GL
胰岛素和收缩都刺激骨骼肌中的葡萄糖转运。胰岛素刺激的葡萄糖转运在肥胖的人类和大鼠中减少。本研究的目的是（1）确定在遗传肥胖的胰岛素抵抗Zucker大鼠的骨骼肌中，收缩刺激的葡萄糖转运是否也受到损害，以及（2）确定先前在瘦受试者的肌肉中观察到的胰岛素和收缩的累加效应是否在肥胖动物的肌肉中明显。为了测量葡萄糖转运，将来自瘦和肥胖Zucker大鼠的后肢在基础、胰岛素刺激（0. 1 μ M）、收缩刺激（坐骨神经的电刺激）和组合的胰岛素+收缩刺激条件。一条后肢被刺激收缩，而对侧腿作为未受刺激的对照。2-在白色腓肠肌、红色腓肠肌和趾长伸肌中测量脱氧葡萄糖转运率。正如预期的那样，与瘦型动物相比，肥胖大鼠三种肌肉中胰岛素刺激的葡萄糖转运速率均显著减慢（P < 0.05）。当表示为基础刺激倍数时，瘦和肥胖动物之间的收缩诱导的肌肉葡萄糖转运率没有显著差异。胰岛素+收缩刺激在瘦动物的骨骼肌中是加和的，但在肥胖动物的骨骼肌中是协同的。先前的收缩增加了肥胖大鼠葡萄糖转运的胰岛素反应性2-5倍，但对瘦对照组的胰岛素反应性没有影响。这种收缩诱导的胰岛素反应性改善可能对肥胖受试者具有临床重要性，可作为改善胰岛素刺激的抵抗性骨骼肌葡萄糖摄取的一种方法。
Both insulin and contraction stimulate glucose transport in skeletal muscle. Insulin-stimulated glucose transport is decreased in obese humans and rats. The aims of this study were (1) to determine if contraction-stimulated glucose transport was also compromised in skeletal muscle of genetically obese insulin-resistant Zucker rats, and (2) to determine whether the additive effects of insulin and contraction previously observed in muscle from lean subjects were evident in muscle from the obese animals. To measure glucose transport, hindlimbs from lean and obese Zucker rats were perfused under basal, insulin-stimulated (0. 1 muM), contraction-stimulated (electrical stimulation of the sciatic nerve) and combined insulin-+contraction-stimulated conditions. One hindlimb was stimulated to contract while the contralateral leg served as an unstimulated control. 2-Deoxyglucose transport rates were measured in the white gastrocnemius, red gastrocnemius and extensor digitorum longus muscles. As expected, the insulin-stimulated glucose transport rate in each of the three muscles was significantly slower (P < 0.05) in obese rats when compared with lean animals. When expressed as fold stimulation over basal, there was no significant difference in contraction-induced muscle glucose transport rates between lean and obese animals. Insulin-+contraction-stimulation was additive in skeletal muscle of lean animals, but synergistic in skeletal muscle of obese animals. Prior contraction increased insulin responsiveness of glucose transport 2-5-fold in the obese rats, but had no effect on insulin responsiveness in the lean controls. This contraction-induced improvement in insulin responsiveness could be of clinical importance to obese subjects as a way to improve insulin-stimulated glucose uptake in resistant skeletal muscle.