Background: Defective branched-chain amino acid (BCAA) catabolism is central to the pathogenesis
of obesity, insulin resistance (IR) and heart disease. Branched-chain α-keto acids
(BCKAs), a catabolic product of BCAAs, is oxidized in the mitochondria by branched-chain
ketoacid dehydrogenase (BCKDH), an enzyme sensitive to inhibitory phosphorylation
by BCKD kinase (BCKDK). BCAAs activate mTORC1, which causes IR by inhibiting insulin
signalling. However, the effect of BCKA on muscle insulin signalling is unexplored.
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