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Dysregulation of branched-chain amino acid (BCAA) metabolism has been shown to be associated with type 2 diabetes mellitus (T2DM) and heart failure. BCAA reportedly protects cells from fatty acid-induced mitochondrial injury via sequestration of fatty acids in intracellular lipid droplets from mitochondria. We previously reported that up-regulation of AMP deaminase 3 (AMPD3) impairs cardiac energetics in T2DM hearts, and AMPD3 was recently shown to participate in regulation of amino acid metabolism in skeletal muscle.

We hypothesized that AMPD3 regulates cardiac amino acid metabolism by interaction with branched-chain α-ketoacid dehydrogenase (BCKDH) complex and that cardioprotective effect of sodium glucose cotransporter 2 inhibitors is mediated by modification of BCAA metabolism in diabetic cardiomyocytes.