Multiple tissue-specific roles for the O-GlcNAc post-translational modification in the induction of and complications arising from type II diabetes.

In this minireview, we will highlight work in the last 30 years that has clearly demonstrated that the O-GlcNAc modification is nutrient-responsive and plays multiple roles in metabolic regulation of signaling and gene expression. Further, we will examine recent studies that have investigated the impact of O-GlcNAc in a variety of glucose- and insulin-responsive tissues and the roles attributed to O-GlcNAc in the induction of insulin resistance and glucose toxicity, the hallmarks of type II diabetes mellitus. We will also summarize potential causal roles for the O-GlcNAc modification in complications associated with diabetes.