Fig. 4: Insulin resistance induced by the HFD can be mitigated by hepatocyte-specific BCL6 overexpression and exacerbated by hepatocyte-specific BCL6 knockout.

A Intraperitoneal glucose tolerance tests (GTTs; 1 g/kg) and (B) intraperitoneal insulin tolerance tests (ITTs; 0.75 U/kg) were performed on the AAV-Control mice and the AAV-BCL6 mice at the 16th week of food administration. The corresponding area under the curve (AUC) of the blood glucose level was calculated (n = 6/group). C Representative western blot analysis (n = 3 western blots for each band) of phosphorylated (p-) and total IRS1, AKT, and GSK3β expression in the livers of the AAV-Control mice and the AAV-BCL6 mice fed an HFD for 16 weeks that received insulin treatment (n = 2 mice in each group without insulin injection; n = 4 mice in each group with insulin injection). D Intraperitoneal glucose tolerance tests (GTTs; 1 g/kg) and (E) intraperitoneal insulin tolerance tests (ITTs; 0.75 U/kg) were performed on the BCL6-CKO and BCL6-flox mice at the 16th week of food administration. The corresponding area under the curve (AUC) of the blood glucose level was calculated (n = 6/group). F Representative western blot analysis (n = 3 western blots for each band) of phosphorylated (p-) and total IRS1, AKT, and GSK3β expression in the livers of the BCL6-CKO and BCL6-flox mice fed an HFD for 16 weeks that received insulin treatment (n = 2 mice in each group without insulin injection; n = 4 mice in each group with insulin injection). Data represent the mean ± SEM, *P < 0.05, **P < 0.01, ***P < 0.001 and n.s. indicates no significance between the two indicated groups.