CHOS (DP: 4) effectively reduced the blood glucose and lipid levels in T2DM mice and improved insulin signaling through the downregulation of PEPCK, FBPase, and G6Pase mRNA gene expression in the IRS/AKT pathway along with the decrease in IRS-1 phosphorylation and an increase in AKT phosphorylation, which promote glycogen synthesis and inhibit gluconeogenesis [104]. This evidence concerns the gene AKT1 and type 2 diabetes mellitus.