Henriksen E J, Ritter L S
Department of Exercise and Sport Sciences, University of Arizona, Tucson 85721.
J Appl Physiol (1985). 1993 Apr;74(4):1653-7. doi: 10.1152/jappl.1993.74.4.1653.
Unweighting of the rat soleus by tail-cast suspension results in increased insulin action on stimulation of glucose transport, which can be explained, at least in part, by increased insulin binding and enhanced glucose transporter protein levels. Glucose transport is also activated by an insulin-independent mechanism stimulated by in vitro muscle contractions or hypoxia. Therefore, the purpose of this study was to determine if soleus unweighting leads to an enhanced response of the insulin-independent pathway for stimulation of glucose transport. The hindlimbs of juvenile male Wistar rats were suspended by a tail-cast system for 3 or 6 days. Glucose transport activity in isolated soleus strips (approximately 18 mg) was then assessed by using 2-deoxy-[1,2-3H]glucose (2-DG) uptake. Insulin (2 mU/ml) had a progressively enhanced effect on 2-DG uptake after 3 and 6 days of unweighting (+44 and +72% vs. control, respectively; both P < 0.001). At these same times, there was no difference between groups for activation of 2-DG uptake by maximally effective treatments with contractions (10 tetanuses), hypoxia (60 min), or caffeine (5 mM). These results indicate that the enhanced capacity for stimulation of glucose transport after soleus unweighting is restricted to the insulin pathway, with no apparent enhancement of the insulin-independent pathway.
通过尾部悬吊使大鼠比目鱼肌失负荷，会导致胰岛素刺激葡萄糖转运的作用增强，这至少部分可以通过胰岛素结合增加和葡萄糖转运蛋白水平升高来解释。葡萄糖转运也可由体外肌肉收缩或缺氧刺激的胰岛素非依赖机制激活。因此，本研究的目的是确定比目鱼肌失负荷是否会导致胰岛素非依赖途径刺激葡萄糖转运的反应增强。将幼年雄性Wistar大鼠的后肢用尾部悬吊系统悬吊3天或6天。然后使用2-脱氧-[1,2-³H]葡萄糖（2-DG）摄取来评估分离的比目鱼肌条（约18mg）中的葡萄糖转运活性。失负荷3天和6天后，胰岛素（2mU/ml）对2-DG摄取的作用逐渐增强（分别比对照增加44%和72%；P均<0.001）。在相同时间，用最大有效收缩（10次强直收缩）、缺氧（60分钟）或咖啡因（5mM）处理激活2-DG摄取时，各组之间没有差异。这些结果表明，比目鱼肌失负荷后刺激葡萄糖转运的能力增强仅限于胰岛素途径，胰岛素非依赖途径没有明显增强。
