Figure 1. Heart Failure in CS-Mpc2−/− mice is not due to energetic stress.

A, Heart weight/tibia length (HW/TL) in CS-Mpc2−/− and fl/fl littermates, n=6. B, Representative gross images of excised fl/fl and CS-Mpc2−/− hearts. Scale bar = 5 mm. C, Heatmap of differentially expressed genes identified by RNA sequencing of hearts from fl/fl and CS-Mpc2−/− littermates, n=3. Most prominently dysregulated KEGG pathways upregulated and downregulated are listed. D through N, mass spectrometry normalized peak area pool sizes of adenosine triphosphate (ATP) (D), adenosine diphosphate (ADP) (E), adenosine monophosphate (AMP) (F), phosphocreatine (G), creatine (H), phosphocreatine/creatine (PCr/Cr) ratio (I), PCr/ATP ratio (J) oxidized nicotinamide adenine dinucleotide (NAD⁺) (K), reduced nicotinamide adenine dinucleotide (NADH) (L), oxidized nicotinamide adenine dinucleotide phosphate (NADP⁺) (M), and reduced nicotinamide adenine dinucleotide phosphate (NADPH) (N) in hearts of fl/fl and CS-Mpc2−/− littermates that had been injected i.p. with U-¹³Cglucose, n=11–12. Data are presented as the mean±SD. Data were evaluated by unpaired, two-tailed Student’s t-test with Welch correction.