Fig. 3

AT-001 reduces myocardial fatty acid oxidation and improves cardiac efficiency in DbCM. (a–f) Glucose oxidation rates (n = 7–9) (a), palmitate oxidation rates (n = 6–8) (b), TCA cycle acetyl CoA production (c), ATP production (d), cardiac work (e), and cardiac efficiency denoted by cardiac work normalized to TCA cycle activity (f) during isolated working heart perfusions from C57BL/6J mice with experimental DbCM at 3 weeks post-treatment with either vehicle control (VC) or AT-001 (40 mg/kg/day). (g–j) Protein expression of LCAD (g), beta-HAD (h), phospho-PDH serine 293 (i), and phospho-AKT serine 473 (j) in myocardial extracts from C57BL/6J mice with experimental DbCM (n = 5) at 3 weeks post-treatment. Values represent means ± SEM. Differences were determined using an unpaired two-tailed Student’s t-test and a two-way ANOVA, followed by a Bonferroni post-hoc analysis. *P < 0.05 significantly different from vehicle control-treated mice. ^#P < 0.05 significantly different from vehicle control-treated mice within palmitate oxidation groups