The major findings of these studies utilizing multiparametric CMR in an HFHSD-induced mouse model of obesity-induced MHD are that SGLT2 inhibition initiated concurrently with the start of an 18-week HFHSD prevented impairment of MPR and diastolic dysfunction, and also prevented the accumulation of EAT volume, CMR proinflammatory EAT biomarkers, and NOS2+ macrophage M1 polarization. This evidence concerns the gene SLC5A2 and obesity disorder.