The energy substrate preference of the human heart is well regulated and is modified upon aging, in that the fetal heart uses glucose, whereas the adult heart utilizes fatty acids. Various human and animal studies suggest a shift in myocardial substrate utilization and decreased rate of myocardial fatty acid uptake and oxidation in heart failure. Given that fatty acids provide greater capacity for energy production compared with glucose, reverting the heart back to using fatty acids might be a therapeutic option for treating heart failure. Targeting the enzymes and/or genes responsible for, or controlling, fatty acid metabolism in the heart, such as peroxisome proliferator-activated receptors (PPARs), mitochondrial fatty acid metabolizing proteins, AMP-activated protein kinase (AMPK), and glucose transporters (GLUTs), could provide novel therapeutic insights for treating heart failure.
ASJC Scopus subject areas
- Drug Discovery