100 If these findings are confirmed, then testing for haptoglobin genotype of all DM patients could be recommended, with addition of vitamin E treatment to reduce ASCVD risk for those with the 2–2 genotype. Genomic approaches (GWAS) not specifically in patients with DM have identified more than 20

variants (SNPs) that are associated with increased risk for coronary artery disease.101 In patients with DM2, a genetic predisposition score derived from GWAS of DM2 predisposition was independently associated with Inhibitors,research,lifescience,medical risk for cardiovascular complications,102 pointing to an overlapping etiological basis for DM2 and ASCVD. However, it is not clear that genomic information enhances the more traditional clinical risk factor approach to ASCVD prediction.103 Nevertheless, genomic studies of coronary artery disease, as with DM2 itself, have potential to improve understanding of pathophysiology, predicttion, Inhibitors,research,lifescience,medical prognosis, diagnosis, and management.104 Studies of Trametinib mouse circulating microRNA in patients with DM found that presence of peripheral vascular complications in DM is associated with loss of endothelial mIR-126, possibly due to disturbed fibrinolysis.26

This field of study has potential to increase understanding Inhibitors,research,lifescience,medical of the pathophysiology of diabetic macrovasculopathy. Proteomic studies of vascular tissue, plaque, and body fluids from patients with atherosclerosis have been performed, with some progress in identifying Inhibitors,research,lifescience,medical potential biomarkers of disease activity or disease risk, as well as proteins of potential pathophysiological significance. Proteomic approaches have identified unusual apolipoprotein patterns in the small dense LDL of insulin-resistant patients with DM and metabolic syndrome that may help explain their susceptibility to ASCVD.105 PERSONALIZED MEDICINE AND DM TREATMENT A goal as yet unrealized in the clinical management Inhibitors,research,lifescience,medical of patients with DM is to use genomic, metabolic, and other data to predict which patients will progress to a particular complication of DM, in order to establish an indication for specific preventive interventions. Within the realm

of preventive therapy, the ideal situation would be the ability to predict individual responsiveness to and tolerance of a particular treatment, in order to CYTH4 design the most effective and best-tolerated individual program of drug, dietary, and exercise therapies. There has been modest progress in understanding the pharmacogenomics of the glucose-lowering medications,37 but practical implementation remains elusive. Thus, choice amongst drugs and drug classes for DM remains largely empirical.8 Compared to the field of pharmacogenomics there has been less research into the genetic determinants of responsiveness to dietary change or increased physical activity, two key modalities in the prevention and treatment of DM. Intriguing recent studies point to differential sensitivity to particular dietary regimens based on genotype.