MCT1 supports mitochondrial lactate use and cardiac resilience in experimental models
Published in Biology, Ischemia, Journals.
Published October 30, 2026.
A Nature study published October 28 identifies a route by which heart mitochondria use lactate as fuel. Researchers found MCT1, a transporter usually associated with the cell surface, in the inner mitochondrial membrane of mouse and human heart-muscle cells.
Working with mitochondrial LDHB, MCT1 supports conversion of lactate into pyruvate and NADH. This provides an alternative entry route for carbohydrate-derived carbon when the mitochondrial pyruvate carrier is absent.
Genetic and biochemical experiments linked loss of MCT1 to impaired lactate oxidation. In mice, losing the transporter worsened adaptation to cardiac stress, including ischemia–reperfusion injury, and accelerated heart failure in the tested models.
The findings help explain metabolic flexibility in the heart, but they do not show that lactate supplementation or a particular drug improves recovery in patients. The authors also note that whole-animal experiments cannot fully separate MCT1’s mitochondrial role from its role at the cell membrane. Human tissue observations support the mechanism without establishing a clinical treatment.
Source: Cluntun et al., Nature. Published October 28, 2026. DOI: 10.1038/s41586-026-11182-3.