Hispidin rescues palmitate‑induced insulin resistance in C2C12 myotubes

Hispidin 可挽救 C2C12 肌管中棕榈酸诱导的胰岛素抵抗

阅读:8
作者:Jong Seok Lee, Jun Myoung Park, Sarah Lee, Hye Jin Lee, Hee-Sun Yang, Joohong Yeo, Ki Rim Lee, Byung Hyun Choi, Eock Kee Hong

Abstract

Skeletal muscle serves an important role in the utilization of glucose during insulin‑stimulated conditions. Excessive saturated fatty acids are considered to be a major contributing factor to insulin resistance in skeletal muscle cells. The present study investigated the effects of hispidin on palmitate‑induced insulin resistance in C2C12 skeletal muscle myotubes via an MTT assay, glucose uptake assay, Oil‑Red‑O staining and western blot analysis. Hispidin reversed the palmitate‑induced inhibition of glucose uptake, and inhibited palmitate‑induced intracellular lipid accumulation. Hispidin suppressed insulin receptor substrate‑1 Ser307 phosphorylation, and significantly promoted the activation of phosphatidylinositol‑3‑kinase and Akt, via inhibition of protein kinase C theta. Furthermore, hispidin treatment of C2C12 muscle cells increased glucose uptake via activation of adenosine monophosphate‑activated protein kinase. These findings indicated that hispidin may improve palmitate‑induced insulin resistance in skeletal muscle myotubes, and therefore hispidin treatment may be beneficial for patients with diabetes.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。