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. 2021 Mar 13;10(6):e018298. doi: 10.1161/JAHA.120.018298

Figure 5. Chronic empagliflozin treatment improved oxidative phosphorylation in failing hearts.

Figure 5

(A) to (D) Mean glucose and oleate acid oxidation, glycolysis, and glucose uptake in isolated perfused hearts from mice in different groups at the end of the protocol (n=5–6). (E) Calculated ATP generation in Sham, Sham+empagliflozin, TAC and TAC+empagliflozin groups (n=5–6). (F) The cardiac output of the isolated perfused hearts (n=5–6) in each group. (G) Left: representative blots of CD36, PPARα, and GAPDH. Right: Quantitative analysis (n=5–6). (H) Left: the representative blots of AMP‐activated protein kinase, acetyl‐coA carboxylase, mammalian target of rapamycin complex 1, S6 ribosomal protein and GAPDH were shown. Right: quantitative analysis (n=5–6). Results are expressed as mean±SEM; One‐way ANOVA (non‐repeated measures) (A–H). ACC indicates acetyl‐coA carboxylase; AMPK, adenosine monophosphate‐activated protein kinase; CD36, cluster of differentiation 36; mTOR, mammalian targe of rapamycin; S6, ribosomal protein S6; and TAC, transverse aortic constriction. *P<0.05 vs sham, † P<0.05 vs transverse aortic constriction.