BCKDHA overexpression redirects amino acids and ketoacids towards mitochondrial oxidation. Limiting intracellular BCAA and BCKA availability prevents amino acid activation of mTOR signalling thereby relieving inhibition on insulin signalling. Notably, BCKDK overexpression do not directly modulate insulin signaling but does promote flux of amino acids into protein synthesis away from mitochondrial oxidation. Acute ketoleucine treatment remodels mitochondrial respiration.