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. 2021 Mar 27;48:101225. doi: 10.1016/j.molmet.2021.101225

Figure 2.

Figure 2

20β-DHB induced both GR- and MR-regulated genes in adipose tissue. (A) The mRNA expression of glucocorticoid receptor (GR), mineralocorticoid receptor (MR), GR-responsive genes patatin-like phospholipase domain-containing 2 (Pnpla2) that encodes adipose triglyceride lipase (Atgl), Tsc22d3 that encodes glucocorticoid-induced leucine zipper protein (GilZ), period 1 (Per1), tumour necrosis factor α (Tnfα), and MR-responsive gene prostaglandin D2 synthase (Ptdgs) (n = 6/group). Data are mean ± SEM. Statistical significance was assessed by the Mann–Whitney U test and two-way ANOVA as appropriate. ∗p < 0.05 relative to the wild-type control. (B) Venn diagram showing overlap of significantly differentially expressed genes (DEGs) in response to aldosterone, dexamethasone, and 20β-DHB in subcutaneous adipose tissue. (C) Scatterplots of DEGs in response to 20β-DHB (red), aldosterone (blue), and both ligands (green). (D) Scatterplots of DEGs in response to 20β-DHB (red), dexamethasone (blue), and both ligands (green). (E) KEGG analysis of the 20β-DHB mediated transcriptome showing the log p value for pathway enrichment. (F) Gene ontology analysis of 20β-DHB mediated transcriptome showing the log p-value for pathway enrichment. (G) Glucose tolerance tests (GTT) in male mice administered 20β-DHB with concurrent vehicle, RU486, or spironolactone (n = 4–5 mice/group) (H) Area under the curve for GTT in the four groups. (I) Fasting plasma glucose concentrations. Data are mean ± SEM. Statistical significance was assessed by ANOVA. ∗p < 0.05 and ∗∗p < 0.01.