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. 2020 May 11;117(21):11674–11684. doi: 10.1073/pnas.1921015117

Fig. 3.

Fig. 3.

Additional ablation of FoxO1 in adipocytes ameliorates metabolic abnormalities of A-PDK1KO mice. (A) Immunoblot analysis of total and Ser256-phosphorylated forms of FoxO1 as well as of total and Thr308-phosphorylated forms of Akt in epididymal adipose tissue of control and A-PDK1KO mice at 10 min after i.p. injection of insulin (5 U/kg) or vehicle. (B) Blood glucose and plasma insulin concentrations in control, A-PDK1KO, or A-PDK1/FoxO1DKO mice at 10 or 20 wk of age (n = 6 to 10). (C) Insulin tolerance test in control, A-PDK1KO, or A-PDK1/FoxO1DKO mice (n = 6 to 8). (D) Immunoblot analysis of Akt phosphorylation in skeletal muscle and liver isolated from control, A-PDK1KO, or A-PDK1/FoxO1DKO female mice at 10 min after i.p. injection of insulin (5 U/kg) or vehicle. (E) Weight and triglyceride content of the liver of control, A-PDK1KO, or A-PDK1/FoxO1DKO mice (n = 5 or 6). (F) H&E staining of liver sections from control, A-PDK1KO, or A-PDK1/FoxO1DKO mice. (Original magnification: 200×.) (G) H&E and Sirius red staining of liver sections from control, A-PDK1KO, or A-PDK1/FoxO1DKO mice at 35 wk to 37 wk of age. (Original magnification: 200×.) All quantitative data are means ± SEM; *P < 0.05, **P < 0.01 for the indicated comparisons or versus corresponding control value (Student’s t test, or ANOVA for comparison of overall time courses in C).