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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。
Objective To study the effect and mechanism of chromium picolinate (CrPic) translocation on fatty acid translocase CD36 of 3T3-L1 adipocytes. Methods 3T3-L1 adipocytes were used as a model. The effects of CrPic and insulin on the translocation of CD36 were observed by immunofluorescence and Western blot. On the basis of this, we explored the molecular mechanism of CrPic on CD36. Results Immunofluorescence results showed that CrPic and insulin promoted the translocation of CD36 from cytosol to cytosolic membrane in 3T3-L1 adipocytes. The results of Western blot showed that the amount of CD36 on the membrane of adipocytes also increased. After administration of compound C, an AMPK pathway inhibitor, the effect of CrPic on CD36 translocation disappeared but the effect of insulin was unaffected. Conclusion CrPic promotes translocation of 3T3-L1 fatty acid translocase CD36 through the AMPK signaling pathway.