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.
Project description:Background & Aims: Non-alcoholic steatohepatitis (NASH), a subtype of non-alcoholic fatty liver disease (NAFLD) that can lead to fibrosis, cirrhosis, and hepatocellular carcinoma, is characterized by hepatic inflammation. Despite evolving therapies aimed to ameliorate inflammation in NASH, the transcriptional changes that lead to inflammation progression in NAFLD remain poorly understood. The aim of this study is to define transcriptional changes in early, non-fibrotic NAFLD using a biopsy-proven non-fibrotic NAFLD cohort. Methods: We extracted RNA from liver tissue of 40 patients with biopsy-proven NAFLD based on NAFLD Activity Score (NAS) (23 with NAS ≤3, 17 with NAS ≥5) and 21 healthy controls and compared changes in expression of 594 genes involved in innate immune function. Results: Compared to healthy controls, NAFLD patients with NAS ≥5 had differential expression of 211 genes, while those with NAS ≤3 had differential expression of only 14 genes. Notably, osteopontin (SPP1) (3.74-fold in NAS ≤3, 8.28-fold in NAS ≥5) and CXCL10 (2.27-fold in NAS ≤3, 8.28-fold in NAS ≥5) gene expression were significantly upregulated with histologic progression of NAFLD.