吡啶羧酸铬通过AMPK信号通路促进3T3-L1脂肪细胞脂肪酸转位酶CD36的转位

Chromium picolinate enhanced CD36 translocation through AMPK pathway in 3T3L1 adipocytes

目的研究吡啶羧酸铬(CrPic)对3T3-L1脂肪细胞脂肪酸转位酶CD36转位的作用及机制。方法采用3T3-L1脂肪细胞作为模型,通过免疫荧光及Western blot等方法观察CrPic及胰岛素对CD36转位的作用;并在此基础上,探讨CrPic对CD36作用的分子机制。结果免疫荧光结果显示CrPic和胰岛素可促进3T3-L1脂肪细胞的CD36从胞质转位到胞膜;Western blot结果表明脂肪细胞胞膜上CD36的含量也增多。给予腺苷酸活化蛋白激酶(AMPK)通路抑制剂compound C之后,CrPic促进CD36转位的作用消失,但胰岛素的作用却不受影响。结论 CrPic通过AMPK信号通路促进3T3-L1脂肪酸转位酶CD36的转位。

AIM To explore the effects and mechanisms of chromium picolinate（CrPic） on CD36 translocation. METHODS Through immunofluorescence microscopy and Western blot,the present study was to investigate the effects and mechanisms of CrPic and insulin on the translocation of CD36 from intracellular storage pools to the plasma membrane （PM） in 3T3-L1 adipocytes.RESULTS Immunofluorescence microscopy and Western blot revealed that upon insulin and CrPic stimulation PM expression of CD36 increased.Furthermore,AMP activated protein kinase（AMPK） inhibitor compound C could abolish the effects of CrPic on CD36 translocation but not insulin.CONCLUSION CrPic increases the translocation of CD36 via the activation of AMPK in 3T3-L1 adipocytes.