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. 2025 Mar 10;301(4):108398. doi: 10.1016/j.jbc.2025.108398

Figure 2.

Figure 2

Effect of PDK1 knockdown on glucose metabolism.A, consumed glucose, (B) intracellular glucose, (C) glycogen abundance was measured in differentiated control and KD cells following 375 μM palmitic acid treatment and nutrient deprivation for 3 h. Control and KD cells were treated with 375 μM palmitic acid treatment for 18 h and (D) glycolytic proton efflux rate, (E) basal glycolytic rate, and (F) compensatory glycolytic rate (G and H) glucose oxidation dependency, (I and J) glucose oxidation capacity and (K–M) ATP production rate were measured from independent cell cultures spanning 3 experimental replicates. Data are shown as mean ± SEM and were analyzed by either a Two-way ANOVA followed by a post hoc Tukey multiple comparison test (A–C) or a two-tailed t test. For (A), ANOVA showed (F and p values) of (3.375 and 0.1035), (113.8 and < 0.0001), (0.02796 and 0.8714) for interaction, row (nutrient availability) and column (cell lines) factors respectively. For (B), ANOVA showed (F and p values) of (1.617 and 0.2323), (40.11 and < 0.0001), (2.083 and 0.1796) for interaction, row (nutrient availability) and column (cell lines) factors respectively. For (C), ANOVA showed (F and p values) of (13.28 and 0.0034), (3.203 and 0.0987), (6.358 and 0.0268) for interaction, row (nutrient availability) and column (cell lines) factors respectively. ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001.