Fig. 7: Trim28 adi-KO alters metabolic gene expression in WAT.

Gene expression analyses performed in gonadal fat pads from female Trim28 wild type (WT) and adipose-specific Trim28 KO (KO) mice fed either a chow or HFD. Imprinted gene network 1 (IGN1) genes Peg3 and Nnat mRNA expression in (a) chow fed, n = 8 WT and n = 7 KO, and (b) HFD-fed mice as determined by qPCR, n = 11/group. Elovl3 mRNA expression in male and female (c) chow-fed mice n = 6 M-WT and n = 10 M-KO, n = 8 F-WT, n = 7 F-KO, and (d) HFD-fed mice n = 9 M-WT and n = 7 M-KO, n = 11 F-WT, n = 11 F-KO. qPCR analysis of gene expression for (e) browning of WAT n = 10 WT and n = 11 KO, and (f) surrogate markers of BAT activity n = 10 WT and n = 11 KO. Volcano plots of differentially expressed genes regulated between chow-fed WT and Trim28 adi-KO mice as determined by RNAseq analysis in gonadal adipose tissue from (g) male mice and (h) female mice. Functional map of genes enriched in WAT from chow-fed Trim28 WT (red) and adi-KO (blue) mice in (i) male and (j) female mice. Enrichment results underwent MSigDB pathway analysis to determine enriched pathways. Gene sets were related by mutual overlap (edge width), where node size is proportional to the total number of genes in each set. Abundance of transcripts determined from RNAseq in WAT of WT and Trim28 adi-KO mice for (k) Elovl family members, and significantly regulated metabolic genes (l) Lpl, Park7, and Pck1, (m) Olr1 and (n) Klf14, (RNAseq: males; n = 6, females; n = 5). All data are represented as mean ± SEM, *p < 0.05 versus WT mice. RNA-seq data were analyzed using ANOVA with FDR correction (Benjamini Hochberg). Specific gene comparisons were analyzed by ANOVA with post hoc testing (Fisher’s LSD).