Normalizing the metabolic phenotype after myocardial infarction: Impact of subchronic high fat feeding

► Previous work has shown high dietary fat (SAT) is cardioprotective post-infarction. ► Energy metabolism changes were evaluated as the potential cardioprotective mechanism. ► SAT increases fatty acid oxidation and reduces glucose oxidation post-MI. ► Pyruvate dehydrogenase regulation is also affected, distinct from SAT or MI alone. ► We conclude SAT after MI improves lipid metabolism to confer cardioprotection.