HK2 and Hyperglycemia: In studies of metabolic dysfunction supporting dicarbonyl stress induced by high glucose concentrations in human aortic endothelial cells and human periodontal ligament fibroblasts in primary culture, we discovered that the increased glucose metabolism driving metabolic dysfunction in model hyperglycemia was mediated by glucose-induced stabilization of HK2 to proteolysis, producing HK2-linked glycolytic overload [13,17].