O-GlcNAcylation is tightly coupled to insulin resistance because hyperglycemia or hyperlipidemia-induced insulin resistance is closely related to altered HBP flux, and in turn, the subsequent aberrant O-GlcNAcylation modifies insulin signaling, glucose uptake, gluconeogenesis, glycogen, and fatty acid synthesis [21]. This evidence concerns the gene INS and Hyperglycemia.