Project description:Liraglutide, a GLP-1 receptor agonist approved for diabetes and obesity, shows promise in treating NAFLD, the most prevalent chronic liver disease globally. Despite its therapeutic potential, the systematic molecular regulations underlying Liraglutide effects on NAFLD remain underexplored, indicating the crucial need to fully understand its mechanism and facilitate its use in NAFLD treatment.Based on this,we established NAFLD modele by feeding C57/BL6 mice a high-fat diet (HFD). After administration of liraglutide injection to HFD mice, liver biochemical parameters were measured to assess the efficacy of liraglutide. Mouse livers were extracted for label-free quantitative proteomics and glycoproteomics analysis to summarize the mechanism of action of liraglutide in ameliorating NAFLD. Meanwhile, liraglutide hydrogels were prepared and characterized to extend the interval of liraglutide injection administration. Our research showed that liraglutide therapeutic effect on NAFLD was largely driven by significant glycosylation changes, which have a more profound impact than changes in overall protein expression. These insights into Liraglutide regulatory networks and targets offered valuable guidance for optimizing NAFLD treatment and advancing its clinical application.
Project description:Despite some success in identifying CNVs responsible for metabolic phenotypes including obesity and diabetes mellitus, there are as yet no data available to suggest whether or not CNVs might be involved in the etiology of the NAFLD spectrum. This report is a comprehensive analysis of copy number in Malaysian patients with NAFLD. Genomic DNA was extracted from blood obtained from patients with NAFLD and submitted for genome-wide analysis using aCGH
Project description:To understand the therapeutic mechanisms of QHD, we examined the effects of QHD treatment on the liver transcriptomes of NAFLD rats and identified multiple therapeutic targets of QHD. We used microarrays to examine the effects of QHD and GC treatment on the liver transcriptomes of NAFLD rats induced by high fat diet and identified multiple therapeutic targets of QHD.
Project description: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.