Presentation description

Mitochondrial carbohydrate oxidation is an important process for cardiac energy metabolism, yet the specific transporters involved remain incompletely understood. Traditionally, the obligate heterodimeric mitochondrial pyruvate carrier (MPC, encoded by Mpc1 and Mpc2) was thought to be responsible for all pyruvate imports for oxidation. However, recent experimental results from the Ducker lab reveals that mitochondrial monocarboxylate transporter 1 (MCT1) allows direct mitochondrial import of lactate, offering an alternative/complementary pathway. Tamoxifen-inducible, cardiomyocyte-specific knockout mice model was used to learn about the role of the mitochondrial pyruvate carrier (MPC1) and monocarboxylate transporter 1 (MCT1) in cardiac carbohydrate oxidation. Deleting MPC1 alone did not reduce TCA cycle labeling from glucose or lactate, due to compensation by mitochondrial lactate import and oxidation via MCT1. In contrast, deleting MCT1 impaired lactate oxidation but maintained glucose oxidation through MPC1. These results suggest that MPC1 and MCT1 provide overlapping pathways to deliver carbohydrate-derived carbons to the TCA cycle—MPC1 imports pyruvate, while MCT1 enables mitochondrial lactate oxidation.