Fig. 4

Notch signaling mediated the glycolytic switch via PI3K/Akt signaling in goose embryonic primary hepatocytes. A Schematic representation of the mechanism by which Notch signaling mediates the glycolytic switch to support avian embryonic growth. B–D Changes in cell morphology (B), cell viability (C), and cell proliferation (D) after being treated with 5 µM DAPT, 20 µM LY294002, or 20 µg/mL 740Y-P (n = 6). E–G Effect of 5 µM DAPT, 20 µM LY294002, or 20 µg/mL 740Y-P on Notch signaling in the goose embryonic primary hepatocytes (n = 6). F, H, and I Relative mRNA expressions of PTEN, PI3K, and Akt (H) and relative protein abundances of PTEN, PI3K, Akt, and p-Akt (F, I) in goose embryonic primary hepatocytes treated with 5 µM DAPT, 20 µM LY294002, or 20 µg/mL 740Y-P (n = 6). F and J–L Effect of 5 µM DAPT, 20 µM LY294002, or 20 µg/mL 740Y-P on glucose consumption, lactate production, ATP levels, oxygen consumption rate (J), and the relative mRNA expressions and protein abundances of HK2, PFK, PKM, and LDHA (F, K and L) in goose primary hepatocytes (n = 6)