...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell biology international. >IRE1 alpha and TRB3 do not contribute to the disruption of proximal insulin signaling caused by palmitate in C2C12 myotubes
【24h】

IRE1 alpha and TRB3 do not contribute to the disruption of proximal insulin signaling caused by palmitate in C2C12 myotubes

机译：IRE1 alpha和TRB3不会导致C2C12肌管中棕榈酸酯引起的近端胰岛素信号的破坏

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Endoplasmic reticulum (ER) stress is a central actor in the physiopathology of insulin resistance (IR) in various tissues. The subsequent unfolded protein response (UPR) interacts with insulin signaling through inositol-requiring 1 alpha (IRE1 alpha) activation and tribbles homolog 3 (TRB3) expressions. IRE1a impairs insulin actions through the activation of c-Jun N-terminal kinase (JNK), and TRB3 is a pseudokinase inhibiting Akt. In muscle cells, the link between ER stress and IR has only been demonstrated by using chemical ER stress inducers or overexpression techniques. However, the involvement of ER stress in lipid-induced muscle IR remains controversial. The aim of the study is to test whether palmitate-induced IRE1a signaling and TRB3 expression disturb insulin signaling in myogenic cells. C2C12 myotubes were exposed to palmitate and then stimulated with insulin. siRNA transfection was used to downregulate TRB3 and IRE1 alpha. Palmitate increased TRB3 expression, activated IRE1a signaling, and reduced the insulin-dependent Akt phosphorylation. Knocking down TRB3 or IRE1a did not prevent the inhibitory effect of palmitate on Akt phosphorylation. Our results support the idea that ER stress is not responsible for lipid-induced IR in C2C12 myotubes.
机译：内质网（ER）应激是各种组织中胰岛素抵抗（IR）的生理病理学的重要角色。随后的未折叠蛋白应答（UPR）通过需要肌醇的1 alpha（IRE1 alpha）激活与胰岛素信号传导相互作用，并使同源物3（TRB3）表达发生变化。 IRE1a通过激活c-Jun N端激酶（JNK）来损害胰岛素作用，而TRB3是抑制Akt的假激酶。在肌肉细胞中，仅通过使用化学内质网应激诱导物或过表达技术就可以证明内质网应激与IR之间的联系。然而，内质网应激在脂质诱导的肌肉IR中的参与仍存在争议。该研究的目的是测试棕榈酸酯诱导的IRE1a信号转导和TRB3表达是否干扰成肌细胞中的胰岛素信号转导。将C2C12肌管暴露于棕榈酸酯，然后用胰岛素刺激。 siRNA转染用于下调TRB3和IRE1 alpha。棕榈酸酯增加TRB3表达，激活IRE1a信号传导，并减少胰岛素依赖性Akt磷酸化。敲低TRB3或IRE1a不能阻止棕榈酸酯对Akt磷酸化的抑制作用。我们的研究结果支持ER应激与C2C12肌管中脂质诱导的IR不相关的想法。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号