The Copenhagen Muscle Research Centre, Molecular Physiology Group, Section of Human Physiology, Department of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark.
Obesity (Silver Spring). 2009 Dec;17 Suppl 3:S15-20. doi: 10.1038/oby.2009.383.
After a single bout of exercise, the ability of insulin to stimulate glucose uptake is markedly improved locally in the previously active muscles. This makes exercise a potent stimulus counteracting insulin resistance characterizing type 2 diabetes (T2D). It is believed that at least part of the mechanism relates to an improved ability of insulin to stimulate translocation of glucose transporters (GLUT4) to the muscle membrane after exercise. How this is accomplished is still unclear; however, an obvious possibility is that exercise interacts with the insulin signaling pathway to GLUT4 translocation allowing for a more potent insulin response. Parallel to unraveling of the insulin signaling cascade, this has been investigated within the past 25 years. Reviewing existing studies clearly indicates that improved insulin action can occur independent of interactions with proximal insulin signaling. In contrast, more recent observations indicate that interactions exist at the distal signaling level of AS160 and atypical protein kinase C (aPKC). Although the functional interpretation is lacking, these novel observations may present a breakthrough in understanding the beneficial interplay between exercise and insulin action.
运动一次后，胰岛素刺激葡萄糖摄取的能力在先前活跃的肌肉中局部显著提高。这使得运动成为一种对抗 2 型糖尿病（T2D）特征性胰岛素抵抗的有效刺激。人们认为，至少部分机制与运动后胰岛素刺激葡萄糖转运蛋白（GLUT4）向肌肉膜易位的能力提高有关。这是如何实现的尚不清楚；然而，一种明显的可能性是，运动与胰岛素信号通路相互作用，促进 GLUT4 易位，从而产生更有效的胰岛素反应。与胰岛素信号级联的阐明并行，这在过去 25 年中进行了研究。回顾现有研究清楚地表明，改善胰岛素作用可以独立于与近端胰岛素信号的相互作用而发生。相比之下，最近的观察结果表明，在 AS160 和非典型蛋白激酶 C（aPKC）的远端信号水平存在相互作用。尽管缺乏功能解释，但这些新的观察结果可能为理解运动与胰岛素作用之间有益的相互作用提供突破。
