Fig. 5: Neutralization or genetic ablation of ACBP results in decreased PPARγ.
From: An obesogenic feedforward loop involving PPARγ, acyl-CoA binding protein and GABAA receptor
A ACBP-neutralizing antibody (α-ACBP) or isotype control (Iso) was administered in vivo by intraperitoneal injection in mice fed with regular-chow (RCD) or high-fat diet (HFD). B Acbp mRNA expression measurement in liver extracts obtained from mice receiving Iso or α-ACBP in RCD or HFD feeding regimens (n = 5 to 9 mice per condition). C Plasma ACBP concentration measurement in Iso—or α-ACBP – treated mice (n = 8 to 10 mice per condition). D, F Liver, epididymal white adipose tissue (eWAT), and brown adipose tissue (BAT) representative immunoblot images of PPARγ and β-actin proteins from mice receiving Iso or α-ACBP (RCD or HFD), densitometric quantification (RCD: n = 5 to 10 mice per condition, HFD: n = 4 to 10 mice per condition) (E, G). H Fasted blood glucose concentration from mice receiving Iso or α-ACBP (RCD or HFD) (n = 5 to 10 mice per condition). I, J eWAT and BAT representative immunoblot images of PPARγ and β-actin proteins from adipocyte-specific ACBP knockout murine model (adipo: Acbp KO) compared to control (adipo: Acbp WT), densitometric quantification (n = 5 to 7 mice per condition) (K, L). Results are displayed as whisker plots (with each dot representing one single mouse) including the mean ± SEM. For statistical analysis p values were calculated by two-tailed unpaired Student’s t-test (C, E, G, K, L) or two-way ANOVA (B, H). a.u. arbitrary units, ns non-significant, kDa kilodaltons. See also Fig. S5.
