Figure 2.

PI3K/AKT Signaling Is Required for Maintenance of Glycolytic Reserve

(A) PI3K-Akt inhibition reduced OxPhos capacity and glycolysis. ECAR data is presented as mean ± SEM; n = 4. The Student t test was used to assess effect of Akt inhibition on ECAR. One-way ANOVA with Tukey’s post-hoc test was used to determine significance in OCR data. (B) PI3K/Akt inhibition reduced cellular ATP levels and ATP generation by glycolysis, but increased the contribution OxPhos to ATP generation. Data is presented as mean ± SD; n = 6; Student t test was used to determine significance. (C and D) Akt inhibition prevented compensatory increase in glucose (¹⁸FDG) uptake and lactate generation following OxPhos inhibition by oligo in glucose medium. Effect of oligo on glucose uptake/lactate generation was examined using the Student t test. Data is presented as mean ± SD; n = 3; Student t test was used to determine significance. (E) Akt inhibition prevented increase in cell surface GLUT1 following OxPhos inhibition by oligo. Data is presented as mean ± SD; n = 6; Student t test was used to determine significance. Cells in the control condition in C to E were treated with vehicle (dimethyl sulfoxide). *p < 0.05; **p < 0.01. Abbreviations as in Figure 1.