Our data support a hypothetical working model in which attenuated BCAA, and possibly cysteine, catabolism contribute to increased blood concentrations of these amino acids and their derivatives in the insulin-resistant state, and we speculate that this contributes to anaplerotic stress that is associated with incomplete oxidation of LCFA and accumulation of acylcarnitines in T2DM. This evidence concerns the gene INS and type 2 diabetes mellitus.