PRRT2 and diabetes mellitus: High glucose levels activate protein kinase C (PKC) and increase both nitric oxide synthase (NOS) and superoxide production in cultured ECs; however, some evidence suggests that PKC-mediated phosphorylation of NOS reduces NO production (Hink et al., 2001), and declines in NO bioavailability coupled with increases in oxidative stress contribute to vascular dysfunction in diabetes.