We found that EMPG not only mimics the effects of the PPARα agonist FF by significantly upregulating key fatty acid oxidation proteins (PPARα, RXRα, and CPT1α) and energy sensors (AMPKα and Sirt1) to promote lipid metabolism but also uniquely suppresses glucose transporter GLUT4 expression and MRGlu, thus reversing the pathological shift of myocardial metabolic substrate toward glycolysis in the HF context. This evidence concerns the gene SLC2A4 and hydrops fetalis.