Several theories of the pathogenesis of microvascular complications of diabetes (diabetic retinopathy, nephropathy, and neuropathy) have been proposed: (1) generation of reactive oxygen species and oxidative stress, (2) activation of polyol pathway, (3) formation of advanced glycation end products, (4) induction of flux through the hexosamine pathway, (5) altered expression and action of growth factors, and (6) activation of protein kinase C. Based on these theories, specific interventions are feasible to prevent the development of diabetic complications even if satisfactory euglycemic control is not achieved.