NOS3 and Hyperglycemia: While our proteomics analysis did not detect a significant difference in HDL-associated apoA-I levels between T2D and controls, other investigators have suggested that hyperglycemia results in nonenzymatic glycation of apoA-I[37] and that glycation of apoA-I, and advanced glycation end-products (AGEs) in general, may contribute to reduction of HDL ability to activate eNOS.[47] Although the T2D patients had elevated glucose and glycated HbA1c, the concentrations we observed only slightly correlated with the ability of HDL to activate eNOS.