FGF21实验结果.zip

We constract HepG2 cells with Vitamin D receptor（VDR）knockdown which mimic the state of vitamin D deficiency in vitro and knock out 1a(OH)ase gene in mice to constract 1,25(OH)2D3 deficiency model in vivo. With 1,25(OH)2D3 deficiency, FGF21 decreased in the liver. Then we found that deficiency of 1,25(OH)2D3 or knockdown of VDR displayed a low phosphorylation of Akt at Ser473 and IRS1 at Tyr895, which mediate the post-insulin receptor signaling pathway. All of this changes, reduced glucose consumption and impaired glycogen synthesis, due to knockdown of VDR or 1,25(OH)2D3 deficiency could be largely reversed with recombinant human FGF21 treatment in vitro. Therefore VDR activation or supplement of vitamin D provoke glycogen synthesis primarily via FGF21.