In a new study, researchers found that high fat or “ketogenic” diets could completely prevent, or even reverse heart failure caused by a metabolic process.
They looked at a metabolic process that seems to be turned down in failing human hearts.
In an animal model, they found drastic heart failure in mice was bypassed by switching to high fat or “ketogenic” diets, which could completely prevent, or even reverse the heart failure.
These suggest that consumption of higher fat and lower carbohydrate diets may be a nutritional therapeutic intervention to treat heart failure.
The research was conducted by a team from Saint Louis University.
The heart’s myocardium requires vast amounts of chemical energy stored in nutrients to fuel cardiac contraction.
To maintain this high metabolic capacity, the heart is flexible and can adapt to altered metabolic fuel supplies during diverse developmental, nutritional, or physiologic conditions.
Impaired flexibility, however, is linked to cardiac dysfunction in conditions including diabetes and heart failure.
The mitochondrial pyruvate carrier (MPC) complex, composed of MPC1 and MPC2, is required for pyruvate import into the mitochondria.
This study showed that MPC expression is decreased in failing human and mouse hearts.
Interestingly, the team found this heart failure can be prevented or even reversed by providing a high-fat, low carbohydrate “ketogenic” diet”.
A 24-hour fast in mice, which is also “ketogenic” also provided strong improvement in heart remodeling.
Diets with higher fat content, but enough carbohydrates to limit ketosis also strongly improved heart failure in mice lacking cardiac MPC expression.
This study reveals a critical role for mitochondrial pyruvate utilization in cardiac function and highlights the potential of dietary interventions to enhance cardiac fat metabolism to prevent or reverse cardiac dysfunction.
The findings suggest that the consumption of higher fat and lower carbohydrate diets may be a nutritional intervention to treat heart failure.
One author of the study is Kyle S. McCommis, Ph.D., an assistant professor in Biochemistry and Molecular Biology.
The study is published in Nature Metabolism.
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