Fig. 4: Genetic inhibition of ACBP/DBI prevents Cushing’s syndrome.
From: Pathogenic role of acyl coenzyme A binding protein (ACBP) in Cushing’s syndrome
a, A scheme showing the experimental schedule of CORT administration in female C57BL/6J mice (Gabrg2F77I/F77I) or wild-type controls (Gabrg2+/+). b–j, Gabrg2F77I/F77I or Gabrg2+/+ mice were treated with CORT (100 μg ml−1 or vehicle control (control) in drinking water, p.o.) for 5 weeks (n = 10, 10, 9 and 10 mice per group): plasma ACBP was measured by ELISA (n = 6 per group) (b), and hepatic Acbp mRNA was assessed by qRT–PCR (n = 6 per group; AU, arbitrary units) (c); average food intake (n = 3 cages per group) (d) and body weight (n = 10, 10, 9 and 10 mice per group) (e) were monitored in the indicated groups (P values compare areas under the curve); the heatmap shows the standardized deviations (z scores) of tissue weights relative to body weight and the quantification of various biochemical parameters across the treatment groups (n = 6 mice per group) (f) (statistical comparisons were performed by pairwise (two-tailed) Wilcoxon test with false discovery rate (FDR) correction for multiple comparisons: P values are indicated); GTT (n = 6 mice per group) (g) and ITT (n = 6 mice per group) (i) were monitored in the indicated groups (the P value represents the comparison of areas under the curve; (GTT (h) and ITT (j)). Statistical comparisons were performed by pairwise Wilcoxon test with FDR correction for multiple comparison in the heatmaps (P values are indicated). All dot plots depict mean ± s.e.m. Two independent repeated experiments were conducted; only one representative result is shown. The curves in d and e were longitudinally analysed with type II ANOVA and pairwise comparisons. The data in b, c, h and j were analysed using one-way ANOVA with Tukey correction. vWAT, visceral white adipose tissue; iWAT, inguinal white adipose tissue; pWAT, perigonadal white adipose tissue; iBAT, interscapular brown adipose tissue. Created with BioRender.com.
