Heart failure is associated with reduced cardiac energetics and this has been linked to impaired substrate utilization. We have assessed in rats how cardiac function and pyruvate dehydrogenase (PDH) flux change upon substrate manipulation, by varying plasma non-esterified fatty acid (NEFA) levels with acipimox injections in both fed and fasted rats. We found that NEFA depletion in fasted rats led to cardiac systolic dysfunction which may be explained by an insufficient compensatory increase in PDH flux boosting glucose oxidation. This model of substrate-manipulation heart failure could be used to assess potential heart-failure drugs in the future.
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