The underlying mechanisms might be bidirectional, with leucine-mediated activation of the mammalian target of rapamycin complex 1 resulting in uncoupling of insulin signaling at an early stage and accumulation of mitotoxic metabolites of branched aminoacids promoting β-cell mitochondrial dysfunction, stress signaling and apoptosis associated with diabetes, and insulin resistance favoring aminoacidemia by increasing the protein degradation that insulin normally suppresses, and/or impairing oxidative metabolism of branched aminoacids in some tissues [44]. Here, INS is linked to diabetes mellitus.