瘦素通过PI3K-PKB-m TOR信号通路调节C2C12肌管蛋白质代谢  

Leptin Regulates Protein Metabolism of C2C12 Myotubes via PI3K-PKB-mTOR Signaling Pathway

作　　者：毛湘冰[1] 陈代文[1] 余冰[1] 何军[1] 虞洁[1] 郑萍[1] 汤俊[1] 谯仕彦[2] 

机构地区：[1]四川农业大学动物营养研究所,动物抗病营养农业部重点实验室,四川雅安625014 [2]中国农业大学动物科技学院,动物营养学国家重点实验室,北京100193

出　　处：《中国畜牧杂志》2014年第3期43-46,共4页Chinese Journal of Animal Science

基　　金：四川省教育厅青年基金项目(10ZB040)

摘　　要：试验旨在探讨瘦素是否通过PI3K-PKB-mTOR信号通路调节骨骼肌细胞蛋白质的代谢。试验以C2C12肌管为研究对象,于无血清DMEM高糖培养基中添加0、100 nmol/L Wortmannin(PI3K活性的抑制剂)或0、20 nmol/L Rapamycin(mTOR活性的抑制剂)预处理45 min后,在培养基中添加0 ng/mL或50 ng/mL重组小鼠瘦素处理2 h,进而测定C2C12肌管内PKB磷酸化水平、mTOR磷酸化水平和蛋白质代谢。结果表明:重组小鼠瘦素处理显著提高了C2C12肌管PKB磷酸化水平、mTOR磷酸化水平和蛋白质合成(P<0.05),显著降低了C2C12肌管蛋白质分解(P<0.05);而Wortmannin或Rapamycin的预处理显著抑制了重组小鼠瘦素对C2C12肌管PKB磷酸化水平或mTOR磷酸化水平的提高,并显著抑制了重组小鼠瘦素对C2C12肌管蛋白质代谢的改善。综上所述,瘦素调节C2C12肌管蛋白质代谢的过程中需要激活PI3K-PKB-mTOR信号通路。The present study was conducted to test the hypothesis that leptin can regulate protein metabolism of skeletal muscles through PI3K-PKB-mTOR signaling pathway. Mouse C2C12 myotubes were utilized as an in vitro model of skeletal muscles. After pre-incubated in serum-free DMEM media containing 100 nmol/L Wortmannin （inhibitor of PI3K activity） or 20 nmol/L Rapamycin （inhibitor of mTOR activity） for 45 min, 50 ng/mL leptin was added to the media. Two hours later, the myotubes were collected to examine PKB phosphorylation state, mTOR phosphorylation state and protein metabolism. The addition of 50 ng/mL leptin stimulated the phosphorylation states of PKB and roTOR, increased the protein synthesis （P〈0.05）, and decreased the protein degradation （P〈0.05）. However, Addition of Wortmannin or Rapamycin to culture medium inhibited leptin-stimulated activation of PKB or roTOR, and decreased leptin-stimulated improvement of protein metabolism in C2C12 myotubes. These results indicate that leptin could affect protein metabolism of skeletal muscles through PI3K-PKB-mTOR signaling pathway.

关 键 词：瘦素 C2C12肌管 蛋白质代谢 PI3K-PKB-mTOR信号通路 

分 类 号：S852.2[农业科学—基础兽医学]