In vivo, this O-GlcNAcylation-induced insulin resistance is mediated, at least in part, by the interaction between phosphatidylinositol 3,4,5-trisphosphate and OGT, which results in the translocation of OGT from the nucleus to the plasma membrane, where the enzyme catalyses dynamic medication of the insulin signaling pathway, including AKT, by O-GlcNAc, attenuating insulin signal transduction (54, 59). Here, INS is linked to Insulin resistance.