Growth hormone excess drives liver aging via increased glycation stress (IMAGE)
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Figure 4. Gly-Low treatment partially reverses transcriptomic alterations induced by GH overexpression. As shown in the experimental regime, bGH-Tg mice were treated with Gly-Low or control diet for 40 weeks, after which liver transcriptomes were analyzed. (A) Venn diagram shows 163 differentially expressed genes (DEGs) overlapping between Gly-Low–treated versus control bGH-Tg mice and bGH-Tg versus WT comparisons. (B) Correlation analysis of shared DEGs demonstrates a strong negative correlation (r = –0.50, p < 0.005), indicating that Gly-Low treatment counteracts transcriptional changes driven by GH excess. (C, D) Analysis of genes downregulated in bGH-Tg mice but restored by Gly-Low revealed enrichment of pathways associated with oxidoreductase activity, adenylate cyclase regulation, estrogen metabolism, and PPAR signaling, with TRRUST implicating transcription factors including SREBF1, ATF6, CLOCK, HNF1A, and NR1I2 as regulators. (E, F) Conversely, analysis of genes upregulated in bGH-Tg mice but suppressed by Gly-Low treatment identified enrichment of pathways related to actin filament–based movement, cAMP-mediated signaling, and gluconeogenesis, with TRRUST highlighting PPARA as a key transcriptional regulator.
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