The following mechanisms have been implicated in age-related development of T2D: (i) defects in insulin signaling (8), (ii) a decrease in insulin-stimulated whole-body glucose oxidation (8), (iii) a reduction in the β-cell response to glucose (8), (iv) impaired insulin-mediated glucose uptake (9), and (v) an inability to suppress hepatic glucose production (9). This evidence concerns the gene INS and type 2 diabetes mellitus.