Fig. 5

Metabolome analysis suggests the abilities of DKG to regulate TCA cycle. A MEFs were treated with 160 μM AscPNa, DHAA, or DKG for three days, and their metabolome profiles were analyzed using 6546 LC/Q-TOF. PCA was performed with the obtained results to visualize the differences in metabolite regulation among the treatments. B–C Volcano plot showing the compounds regulated by DKG compared to the control B. Changes in these compounds by DHAA and AscPNa treatments were summarized C. D The abilities of AscPNa, DHAA, and DKG to regulate canonical TCA cycle were analyzed. E Inhibition of canonical TCA cycle resulted in an increase in succinate, fumarate, and malate, while α-KG levels decreased. F–G The effects of 160 μM AscPNa, DHAA, and DKG on ECAR and OCR were determined using the Seahorse instrument. H–K During reprogramming, MEFs were treated with 160 μM AscPNa, DHAA, or DKG. The concentrations of succinate H and α-KG I, glycolysis J, and ATP production through oxidative phosphorylation (OXPHOS) K were determined on day 3. Metabolome analysis was performed at least eight times (n ≥ 8), while other experiments were repeated at least five times (n ≥ 5). Additional statistical information is listed in Additional file 4: Table S3. For related information, see also Additional file 1: Figure S3