Preliminary Study of the Mechanism of Fenofibrate in the Treatment of Nonalcoholic Fatty Liver Disease based on Bioinformatic Analysis

The aim of this study was to explore the possible action mechanism of fenofibrate in treating non-alcoholic fatty liver disease (NAFLD) through bioinformatic analysis. Statistical and bioinformatic analyses were conducted through Gene Ontology, Gene Set Enrichment Analysis (GSEA), and Kyoto Encyclopedia of Genes and Genomes (KEGG). The control, high-fat diet (HFD), and HFD + fenofibrate (HFD + Fen) groups were analyzed for differentially expressed genes (DEGs). In the HFD versus control dataset analysis, 493 DEGs were identified, of which 200 were upregulated and 293 were downregulated. In the HFD + Fen versus HFD dataset, 449 DEGs, comprising 376 upregulated and 73 downregulated genes, were observed. Two KEGG pathways and one key gene were identified. The key gene mup family appeared to mediate the mechanism underlying NAFLD. Treatment of NAFLD with fenofibrate may occur through the core gene mup. Overall design: Thirty mice were randomly assigned to a control group (n = 10), high-fat group (n = 10), and fenofibrate treatment group (n = 10). The high-fat and fenofibrate treatment groups received a 14-week high-fat diet intervention. The control group was on a normal diet for 14 weeks. After 10 weeks, the fenofibrate treatment group received fenofibrate gavage treatment, and then continued to receive a high-fat diet for 4 weeks. After 14 weeks, the liver tissues were collected. RNA/DNA extraction was performed to build a library, and liver transcriptome sequencing (RNA-Seq) was performed.