Liver Transcriptomics Reveals UB-NPs Regulate Lipid Metabolism and Inflammation Genes

This study utilized RNA-Seq to investigate hepatic gene expression changes in obese mice following intervention with UB-NPs, based on prior evidence indicating the liver as a primary site of UB metabolism. High-quality sequencing data (Q30 > 95.93%, alignment efficiency 90.69–97.47% to GRCm39) revealed 3,387 differentially expressed genes (DEGs) between UB-NPs and high-fat diet (HFD) groups, including 687 overlapping DEGs with the HFD vs. normal diet comparison. Among these, 570 DEGs showed expression reversal patterns, indicating potential key targets of UB-NPs. Functional enrichment analyses (GO, Reactome, KEGG) demonstrated that UB-NPs significantly modulate genes involved in lipid and fatty acid metabolism, mitochondrial beta-oxidation, TCA cycle, inflammatory pathways (e.g., NF-kappa B), and PPAR signaling. UB-NPs upregulated fatty acid oxidation genes (e.g., Ppara, Ehhadh, Cyp4a14) and downregulated pro-inflammatory genes (e.g., Tnf, Traf1). These results suggest UB-NPs ameliorate obesity-related metabolic dysregulation by enhancing lipid catabolism and suppressing inflammation.