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首页> 外文会议>Canadian Veterinary Medical Association Convention >ROLE OF AMPK IN SKELETAL MUSCLE: FROM METABOLIC SIGNALING TO IMMUNE REGULATION
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ROLE OF AMPK IN SKELETAL MUSCLE: FROM METABOLIC SIGNALING TO IMMUNE REGULATION

机译：AMPK在骨骼肌中的作用：从代谢信号传递到免疫调节

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Skeletal muscle is the major tissue responsible for whole-body glucose disposal when insulin levels rise after a meal and during physical exercise. It is now well established that the translocation of GLUT4 glucose transporters from intracellular compartments to the cell surface represents an important mechanism by which both insulin and exercise stimulate glucose transport in muscle cells. Furthermore, there is now substantial evidence that impaired insulin stimulation of glucose transport in skeletal muscle of type 2 diabetic individuals is mainly caused by a defect in insulin receptor signaling to the PBK/Akt pathway, leading to impaired GLUT4 translocation and/or activation of the transporter protein at the cell surface. Importantly, the effectof exercise/contraction on glucose transport appears to be relatively well preserved in diabetic muscle. It is therefore critical to fully understand the signaling mechanisms that induce glucose transport in skeletal muscle of exercised/contracted muscles, with the hope of discovering novel targets for the treatment of muscle insulin resistance in type 2 diabetic subjects. Muscular contraction activates 5'-AMP-activated protein kinase (AMPK) and there is accumulating evidence that this energy-sensing enzyme mediates at least part of the metabolic effects of exercise. Because activation of AMPK also increases lipid oxidation in muscle, it is considered to be largely responsible for the health benefits of exercise and is thought to be a promising targetfor the development of new treatments for obesity, insulin resistance and type 2 diabetes.
机译：骨骼肌是当胰岛素水平和体育锻炼后胰岛素水平上升时，负责全身葡萄糖处理的主要组织。现在已经确定，从细胞内隔室转移到细胞表面的Glut4葡萄​​糖转运蛋白代表了胰岛素和运动刺激肌肉细胞中葡萄糖输送的重要机制。此外，现在有大量的证据表明，在2型糖尿病的个体的骨骼肌葡萄糖转运的受损的胰岛素刺激的主要原因是在胰岛素受体信号到PBK / Akt途径的缺陷，导致受损的GLUT4易位和/或活化在细胞表面的转运蛋白。重要的是，在糖尿病肌肉中似乎对葡萄糖运输的运动/收缩似乎相对较好。因此，充分了解诱导葡萄糖肌肉肌肉肌肉肌肉肌肉肌肉的信号传导机制至关重要，希望发现新的糖尿病受试者治疗肌肉胰岛素抵抗的新靶标。肌肉收缩激活5'-AMP活化的蛋白激酶（AMPK），并且积累了累积的证据，即这种能量传感酶介导运动的至少一部分代谢效果。由于AMPK的活化也增加了肌肉中的脂质氧化，因此认为对运动的健康益处主要负责，并且被认为是开发肥胖，胰岛素抵抗和2型糖尿病新治疗的有前途的目标。

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