The objective of our current study is to evaluate the protection conferred by oral SFN administration against DCM in the diabetic db/db mouse model from structural, morphological, and functional perspectives, and to explore mechanistic implications in terms of systemic metabolic improvements (blood biochemistry, adiposity, and MAFLD), as well as local modulation of cardiac substrate metabolism (cardiac abundance of CD36, H-FABP, FATP4, GLUT4, CPT1B, MPC1, MPC2, PDK4, and PPARα) and mitochondrial functions (ATP production and activity of mitochondrial respiratory chain enzymes). This evidence concerns the gene CD36 and familial dilated cardiomyopathy.