HFD disrupts autophagy and metabolism in adipose FoxO1 KO mice.

(A) The strategies of dietary and tamoxifen treatments; CTH stands for chow→ tamoxifen→HFD, and HTH stands for HFD→ tamoxifen→HFD. (B) Measurements of body weight after the control and adO1KO mice were treated by CTH and HTH; n=8–12. (C) Measurements of fat mass after the control and adO1KO mice were treated by CTH and HTH; n=8–12. (D,E) Glucose tolerance test for the control and adO1KO mice treated by CTH (D) and HTH (E); n=6. (F,G) Western blotting (F) and densitometric (G) analyses of autophagy proteins in inguinal adipose tissues from CTH-treated mice; n=6. (H,I) Western blotting (H) and densitometric (I) analyses of mitophagy adaptor (Pink1) and receptors (Bnip3 and Fundc1) in inguinal adipose tissues from CTH-treated mice; n=6. (J) Western blotting (upper panel) and densitometric (lower panel) analyses of adipose browning maker UCP1 in inguinal adipose tissues from CTH-treated mice; n=6. (K–M) Measurement of basal respiration (BR, K), maximal respiration (MR, L), and spare respiration capacity (SRC, M) of 3T3L1 adipocytes treated with vehicle DMSO, FoxO1 inhibitor AS, and autophagy inhibitor Baf (i.e., bafilomycin A1); n=3–4; *P<0.05, **P<0.01, ***P<0.001; n.s., not significant.