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首页> 外文期刊>Life sciences >A role for calcium/calmodulin kinase in insulin stimulated glucose transport
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A role for calcium/calmodulin kinase in insulin stimulated glucose transport

机译：钙/钙调蛋白激酶在胰岛素刺激的葡萄糖转运中的作用

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Previous research has shown that the CAMK (calcium/calmodulin dependent protein kinase) inhibitor, KN62, can lead to reductions in insulin stimulated glucose transport. Although controversial, an L-type calcium channel mechanism has also been hypothesized to be involved in insulin stimulated glucose transport. The purpose of this report was to determine if 1) L-type calcium channels and CAMK are involved in a similar signaling pathway in the control of insulin stimulated glucose transport and 2) determine if insulin induces an increase in CAMKII phosphorylation through an L-type calcium channel dependent mechanism. Insulin stimulated glucose transport was significantly (p<0.05) inhibited to a similar extent (&SIM;30%) by both KN62 and nifedipine in rat soleus and epitrochelaris muscles. The new finding of these experiments was that the combined inhibitory effect of these two compounds was not greater than the effect of either inhibitor alone. To more accurately determine the interaction between CAMK and L-type calcium channels, we measured insulin induced changes in CAMKII phosphorylation using Western blot analysis. The novel finding of this set of experiments was that insulin induced an increase in phosphorylated CAMKII (&SIM;40%) in rat soleus muscle that was reversed in the presence of KN62 but not nifedipine. Taken together these results suggest that a CAMK signaling mechanism may be involved in insulin stimulated glucose transport in skeletal muscle through an L-type calcium channel independent mechanism. (C) 2003 Elsevier Inc. All rights reserved. [References: 33]
机译：先前的研究表明，CAMK（钙/钙调蛋白依赖性蛋白激酶）抑制剂KN62可导致胰岛素刺激的葡萄糖转运减少。尽管存在争议，但还假设L型钙通道机制与胰岛素刺激的葡萄糖转运有关。本报告的目的是确定1）L型钙通道和CAMK是否参与控制胰岛素刺激的葡萄糖转运的类似信号通路，以及2）确定胰岛素是否通过L型诱导CAMKII磷酸化的增加钙通道依赖性机制。 KN62和硝苯地平在大鼠比目鱼肌和上chel肌中均显着（p <0.05）抑制胰岛素刺激的葡萄糖转运（pSIM <30％）。这些实验的新发现是这两种化合物的联合抑制作用不大于单独一种抑制剂的作用。为了更准确地确定CAMK和L型钙通道之间的相互作用，我们使用蛋白质印迹分析测量了胰岛素诱导的CAMKII磷酸化变化。这组实验的新发现是胰岛素诱导大鼠比目鱼肌中磷酸化CAMKII（＆SIM; 40％）的增加，这种增加在存在KN62而不是硝苯地平时被逆转。总之，这些结果表明，CAMK信号传导机制可能通过L型钙通道独立机制参与胰岛素刺激的骨骼肌葡萄糖转运。 （C）2003 Elsevier Inc.保留所有权利。 [参考：33]

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