The focus of our work is myocardial energy metabolism. Energy is the capacity for doing work. Our work is built on the premise that the heart is an efficient energy converter. Like skeletal muscle, heart muscle employs different mechanisms to adapt to acute and to sustained changes in energy demand.
Immediate adaptation involves reactions for which the organ has ready-made mechanisms in place.
The mechanisms include the instantaneous downregulation of substrate metabolism with a decrease in cardiac work, and the sudden, selective increase in glycogenolysis and glucose oxidation with an increase in cardiac work. We propose that energy substrate metabolism forms the link between gene expression and contractile function of the heart. We have examined the metabolic consequence of hypertrophy and atrophy in our isolated working heart preparation. This approach revealed a shift of substrate preference from fatty acids to glucose, and in an absent response to insulin. A major emphasis of our work is on metabolic signals that regulate cardiac gene transcription, that alter cardiac function, and that may become targets for drugs.