High dietary fat promotes a normal metabolic phenotype in the infarcted rat heart

Abstract

Lipid accumulation is suspected to induce & exacerbate cardiac dysfunction. However, work in our lab has shown high dietary fat (SAT) subsequent to myocardial infarction results in less dysfunction as compared to a standard diet despite increased tissue lipids. This is accompanied by improved mitochondrial function suggesting SAT protection involves energy metabolism. This study sought to evaluate whether SAT alters the energy substrate utilization profile after cardiac infarction. Coronary ligated (HF) or sham (SH) rats were fed SAT or normal chow (NC) for 8 weeks. Working heart perfusions were performed to evaluate function (output, heart rate, & oxygen uptake) & metabolism (glucose & fatty acid oxidation) at low & high workloads. At low workload, cardiac output & oxygen uptake were decreased & glucose oxidation was increased in HF‐NC, but not in HF‐SAT. High workload data suggest a similar trend, but the protective effects were diminished. Lower oxygen use & increased glucose reliance implies a switch from fatty acids in the HF‐NC hearts, a hallmark of heart failure. However, the lack of these differences in the HF‐SAT at low workload suggests SAT does indeed modulate energy metabolism of the infarcted heart. This work supports the hypothesis that high dietary fat after infarction promotes a normal metabolic phenotype & is part of the mechanism by which high fat is protective of cardiac function.