“…In HF following cardiac hypertrophy, there is a major metabolic switch in myocardial substrate metabolism from fatty acid to glucose oxidation. [2][3][4][5] A key marker of this switch is the coordinated downregulation of fatty acid oxidation enzymes (eg, medium-chain acyl-CoA dehydrogenase and carnitine palmitoyltransferase-I β) and mRNA levels in the human LV with a concomitant increase in glucose uptake and oxidation. 2,6 This switch is thought to represent a metabolic reprogramming toward substrate metabolism that is more commonly seen in the fetal heart.…”