MCT1-dependent mitochondrial lactate import sustains cardiac metabolism.

MCT1-dependent mitochondrial lactate import sustains mouse myocardium metabolism when the mitochondrial pyruvate carrier is genetically ablated, enabling glucose-derived carbon oxidation via lactate.

• Why it matters: The heart’s fuel flexibility depends on mitochondrial carbohydrate entry, but it is unclear how glucose oxidation persists when MPC is absent under dietary, exertion, and injury stressors.
• What they did: Using genetic and pharmacological tools, the study shows MCT1 (Slc16a1) is required for glucose carbon oxidation by MPC-deficient myocardium, and that MCT1 localizes to the inner mitochondrial membrane in mouse and human cardiomyocytes.
• The result: Loss of MCT1 impairs lactate oxidation, disrupts metabolic flexibility, and accelerates heart failure development with increased mortality after hyperactivation of the neurohormonal axis or ischemia-reperfusion injury.

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