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. 2020 Jan 8;6:186. doi: 10.3389/fcvm.2019.00186

Figure 2.

Figure 2

SGLT2 inhibitors increase the amount of ketone bodies, thereby promoting cardioprotective effects. The inhibition of SGLT2 reduces plasma glucose levels, thereby promoting lipolysis in adipose tissue, which in turn enhances the generation of ketone bodies. On the other hand, a growing body of evidence suggests that ketone bodies are favorable substrates in energy production because the conversion of ketone bodies to acetyl-CoA is much easier in comparison to the conversion of FFAs and glucose to acetyl-CoA. Furthermore, transcriptional level changes of ketone oxidation-related genes would be associated with the substrate shift to ketone bodies in the failing heart. Both pink and blue arrows show the changes in heart failure. AcAc CoA, Acetoacetyl CoA; ACAT1, Acetyl-CoA acetyltransferase; ADP, Adenosine diphosphate; ATP, Adenosine triphosphate; BDH1, Mitochondrial β-hydroxybutyrate dehydrogenase; βOHB, β-hydroxybutyrate; βOHB CoA, β-hydroxybutyryl CoA; C2-carnitine, Acetylcarnitine; C4-OH carnitine, Hydroxybutyrylcarnitine; CPT1, Carnitine palmitoyltransferase 1; ETC, Electron transport chain; HMGCL, 3-hydroxy-3-methylglutaryl-coenzyme A lyase; HMGCS2, 3-hydroxy-3-methylglutaryl-coenzyme A synthase 2; and SCOT, Succinyl-CoA:3-oxoacid-CoA transferase.