The underlying mechanism by which HUA leads to AN may include the following points: firstly, high serum UA induced oxidative stress and increased reactive oxygen species (ROS) levels; secondly, elevated ROS levels subsequently activated phospho-insulin receptor substrate-1 (IRS-1) (Ser307/312) and then inhibited phospho-Akt (Ser473), which finally inhibited the downstream transduction of insulin signaling and led to insulin resistance [30]. This evidence concerns the gene AKT1 and Insulin resistance.