Fig. 5: Hmgcs2 and ketone body β-HB are essential for FA-stimulated metabolic reprogramming in neonatal mouse heart.

a qPCR detection of the mRNA levels of FA metabolism-related genes in NRVMs treated with BSA or FA (n = 5 for each group). b qPCR detection of the mRNA levels of glycolytic metabolism-related genes in NRVMs treated with BSA or 200 μM FA (n = 5 for each group). c Extracellular metabolic flux analysis of the mitochondrial OCR in negative control (NC) and Hmgcs2-silenced (si-H2) NRVMs treated with BSA or 200 μM FA (n = 4–5 for each group). d Extracellular metabolic flux analysis of the mitochondrial OCR in WT and KO neonatal mouse ventricular myocytes (NMVMs) treated with PBS or 5 mM β-HB for 24 h (n = 5 for each group). e Extracellular metabolic flux analysis of extracellular acidification rate (ECAR) in WT and KO NMVMs (n = 5 for each group). f Lactate levels in the hearts of P5d WT and KO mice (n = 4–5 for each group). g Pyruvate levels in the hearts of P5d WT and KO mice (WT, n = 9; KO, n = 6). h Relative ATP levels in the hearts of P5d WT and KO mice (WT, n = 10; KO, n = 7). i Glucose oxidation capacity of the cardiomyocytes in WT and KO mice at P5d was detected by an extracellular metabolic flux analyzer (n = 6 for each group). j FA oxidation capacity of the cardiomyocytes in WT and KO mice at P5d was detected by an extracellular metabolic flux analyzer (n = 6 for each group). k–p qPCR detection of embryonic marker gene expression in the hearts of WT and KO mice. Data are presented as means ± SEM. and the P values were determined by unpaired two-tailed Student’s t-test. *P < 0.05; **P < 0.01; ***P < 0.001.