Fig. 4: Liver-specific PPARγ knockout yields decreased ACBP levels.
From: An obesogenic feedforward loop involving PPARγ, acyl-CoA binding protein and GABAA receptor
A Pparg mRNA expression (n = 5 to 15 mice per condition) and B, C protein level measurements (n = 4 to 7 mice per condition) in liver extracts obtained from control (PPARγ WT) or liver-specific CRISPR/Cas9-mediated PPARγ-knockdown mice (PPARγ KD) receiving regular-chow (RCD) or high-fat diet (HFD). For statistical analysis (C) p values were calculated comparing HFD groups to the corresponding RCD group for each genetic background (PPARγ WT, PPARγ KD). D Acbp mRNA expression (n = 5 to 13 mice per condition), E plasma ACBP concentration (n = 5 to 15 mice per condition), and F body weight gain measurements in control or PPARγ KD mice rendered obese (HFD, 2 months) (n = 9 to 10 mice per condition). G Representative hematoxylin eosin (HE) images of control or PPARγ KD livers (n = 15 to 25 mice per condition) obtained from mice receiving RCD or HFD, hepatosteatosis score quantification (bar: 50 μm, ND non-detected) (H). I Fasted blood glucose concentration from control or liver-PPARγ KD mice receiving RCD or HFD (n = 9 to 10 mice per condition). 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), two-way ANOVA (A, D–F, I), or Mann–Whitney test (H). kDa kilodaltons, a.u. arbitrary units, ns non-significant, ND non-detected. See also Fig. S4.
