Abstract
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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