Editorial Focus PDC deletion: the way to a man’s heart disease

THE HEART HAS continuous high-energy demands required to sustain efficient contraction. This is met by the metabolism of major circulating substrates (e.g., glucose, lactate, or lipids), according to availability, since the heart has a limited capacity for nutrient storage (reviewed in Ref. 16). Although fatty acid (FA) oxidation rates are invariably higher than glucose oxida-tion rates, glucose oxidation is more energy efficient than FA oxidation (with 15 % more ATP/O2 molecule). Glucose and lipids compete as oxidative substrates for the heart, resulting in either a glucose-FA cycle in which lipid predominates as oxidative substrate or a reverse glucose-FA cycle in which lipid oxidation may be suppressed and glucose utilization favored. In addition, cardiac fuel selection is modified in disease states. Cardiac hypertrophy and heart failure, often characterized by reexpression of fetal genes, can be associate