Regulation of exercise-stimulated glucose uptake in skeletal muscle.
Regulation of exercise-stimulated glucose uptake in skeletal muscle.
复制标题
DOI：
10.6065/apem.2016.21.2.61
复制
发表时间：
2016-06
影响因子：
2.2
通讯作者：
Koh HJ
中科院分区：
文献类型：
--
作者：
Koh HJ
AMPK（AMP-activated protein kinase）是一种丝氨酸/苏氨酸激酶，被认为是运动刺激骨骼肌葡萄糖摄取的重要介质。肝激酶B1（LKB 1）是AMPK和AMPK相关蛋白激酶的上游激酶，其在骨骼肌中的功能尚未得到很好的证明。我们的团队和其他人已经产生了骨骼肌中缺乏AMPK活性的小鼠，以及肌肉特异性LKB 1敲除小鼠。本文就AMPK和LKB 1在调节运动性骨骼肌葡萄糖摄取中的作用进行综述。我们还讨论了我们最近的研究，展示了肥胖诱导的骨骼肌胰岛素抵抗的分子机制。
AMP-activated protein kinase (AMPK) is a Ser/Thr kinase that has been thought to be an important mediator for exercise-stimulated glucose uptake in skeletal muscle. Liver kinase B1 (LKB1) is an upstream kinase for AMPK and AMPK-related protein kinases, of which the function in skeletal muscle has not been well documented. Our group and others have generated mice lacking AMPK activity in skeletal muscle, as well as muscle-specific LKB1 knockout mice. In this review, we discuss the potential role of AMPK and LKB1 in regulating exercise-stimulated glucose uptake in skeletal muscle. We also discuss our recent study, demonstrating the molecular mechanism of obesity-induced development of skeletal muscle insulin resistance.