Editorial Metabolic Remodeling in the Hypertrophic Heart Fuel for Thought

When it comes to fuel for energy production, it iscommonly accepted that the heart is an omnivore, capable of oxidizing a wide range of carbon substrates, and that this metabolic plasticity is necessary to maintain a high and variable workload in the midst of an ever-changing hormonal and nutritional state.1 It is also widely appreciated that shifts in substrate utilization in the heart occur in response to chronic metabolic and hemodynamic stresses.2–5 What is less clear, however, is whether such chronic meta-bolic shifts should be considered a cause or consequence in the pathogenesis of contractile dysfunction. In the case of diabetes mellitus, the heart exhibits an increased dependence on fatty acids for oxidative energy production, and this increase in lipid metabolism has been proposed to signifi-cantly contribute to the etiology of impaired cardiac func-tion.6 Similarly, increased rates of fatty acid oxidation imme