In contrast, we analyzed human plasma samples as well as determined the relationship between accumulated ADMA and insulin resistance with using cell and mouse models; ADMA treatment on C2C12 myotubes inhibits its degrading enzyme DDAH thus leads to accumulation of it, and in the end could attenuate insulin signaling and subsequent glucose uptake in skeletal muscle, the major organ of glucose disposal14. This evidence concerns the gene DDAH1 and Insulin resistance.