Additionally, experimental studies have shown that cardiac glycolipid toxicity, impaired insulin signaling, cardiac energetic impairment, activation of the renin–angiotensin system (RAS) and increased formation of angiotensin II (Ang II), cardiac autonomic neuropathy, reduced NO bioavailability, elevations in AGEs, and dysregulated cardiomyocyte calcium handling, play central roles in diabetic cardiomyopathy pathologies (Figure 1) (Pechánová et al., 2015; Jia et al., 2018a; Jia et al., 2018b; Dhalla and Shah, 2020; Komici et al., 2019; Zamora and Villena, 2019). Here, INS is linked to diabetic cardiomyopathy.