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Distinct hepatic gene expression patterns characterize progressive disease in NAFLD

ABSTRACT: The pathogenesis of non-alcoholic fatty liver disease is not fully understood. Transcriptomic analysis of a large cohort of 318 patients provides evidence of gene perturbations related to inflammation, complement and coagulation pathways, and tissue remodeling in distinct states of NAFLD.

ORGANISM(S): Homo sapiens

PROVIDER: GSE163211 | GEO | 2021/10/15

REPOSITORIES: GEO

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Distinct hepatic gene expression patterns characterize progressive disease in NAFLD

Project description:Distinct hepatic gene expression patterns characterize progressive disease in NAFLD

| PRJNA685198 | ENA

FLORINASH - The role of intestinal microflora in non-alcoholic fatty liver disease (NAFLD) EU FP7-HEALTH, project number 241913

Project description:FLORINASH - The role of intestinal microflora in non-alcoholic fatty liver disease (NAFLD) EU FP7-HEALTH, project number 241913<br>Florinash examined the role on the gut microbiota in NAFLD. Metagenomic, proteomic, metabolomic and transcriptomic data were integrated to give provide a systems biology approach to disease-associated studies. Liver biopsies were obtained from patients undergoing bariatric surgery; one was used to diagnose NAFLD, the other was used to examine the host transcriptome in NAFLD. This dataset is part of the TransQST collection.

2018-03-15 | E-MTAB-4856 | biostudies-arrayexpress

Effects of NAFLD/NASH on hepatic gene expression.

Project description:To characterize gene expression changes in arachidonic acid metabolism pathway genes in the presense of non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH) mice administered were administered an atherogenic diet for a period of four weeks. Administration of the atherogenic diet resulted in significant enrichment of the arachidonic acid metabolism pathway by gene set enrichment analysis (GSEA). The core enrichment subset of genes was down-regulated in mice administered the atherogenic diet and the majority of the genes that were down-regulated were cytochrome P450s. A total of 4 wild-type mice were administered a standard diet (STD; control group) and 4 wild-type mice were administered a HFHC diet (HFHC).

2014-01-03 | E-GEOD-53381 | biostudies-arrayexpress

Transcriptional analysis of non-fibrotic NAFLD progression

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.

2020-07-08 | GSE151158 | GEO

Effect of GCN5 depletion in hepatocytes in NAFLD

Project description:Non-alcoholic fatty liver disease (NAFLD) is a burden of global health, yet the mechanism of the disease is not fully elucidated. General control non-repressed protein 5 (GCN5) is histone acetyltransferases. We invesgated the effect of GCN5 deletion on gene expression in a NAFLD cell model.

2024-10-23 | GSE279791 | GEO

Prognostic Liver Signature for NAFLD (PLS-NAFLD) profiles of cell-based PLS system treated with free fatty acids (FFA) and IDO1 inhibitor, epacadostat.

Project description:Non-alcoholic fatty liver disease (NAFLD), alongside the global obesity epidemic, is rapidly emerging as a dominant liver disease etiology that leads to progressive liver fibrosis, its terminal stage, cirrhosis, and hepatocellular carcinoma (HCC). We identified and validated a 133-gene signature (Prognostic Liver Signature for NAFLD [PLS-NAFLD]) to predict long-term HCC risk in patients with NAFLD. By analyzing PLS-NAFLD, IDO1 was identified as a potenial chemopreventive target for HCC from NAFLD. To test this hypothesis, we utilized our clinical-prognostic-signature-inducible cell culture model. We first confirmed that free fatty acid treatment (800 μM oleic acid and 400 μM palmitic acid) can induce PLS-NAFLD, then IDO1 inhibitor, epacadostat, can reverse the high-risk pattern in a dose-dependent manner.

2022-07-01 | GSE200460 | GEO

Lack of associations of microRNAs with severe NAFLD in people living with HIV: Discovery case-control study

Project description:The aim of this discovery case-control study was to identify patterns of differential expression of microRNAs in people living with HIV (PLWH) and assess their diagnostic value for non-alcoholic fatty liver disease (NALFD). Cases were defined as patients with severe NAFLD and controls as patients without NAFLD, characterized using the controlled attenuation parameter (CAP). Cases and controls were matched 1:1 for age, sex, body mass index, CD4+ lymphocyte count, active HCV infection, and ART regimen. Serum 2,083 simultaneous microRNA transcripts were analyzed using HTG technology and compared between cases and controls. Forty-five patients, 23 cases, and 22 controls were included in the study. In the analysis of the expression pattern of the 2,083 microRNAs, no differential expression patterns were found between both groups of patients included in the study. Analysis of the microRNA transcriptome profile of nonobese PLWH with severe NAFLD did not appear to differ from that of patients without NAFLD. Thus, microRNA might not serve as a proper biomarker for predicting severe NALFD in this population.

2023-05-03 | E-MTAB-12974 | biostudies-arrayexpress

Single Nuclei RNA-Seq to map progression of non-alcoholic fatty liver disease (NAFLD) in patients II

Project description:Non-alcoholic fatty liver disease (NAFLD) is of increasing prevalence and concern. NAFLD can progress to non-alcoholic steatohepatitis (NASH), to cirrhosis and finally to end-stage liver disease where liver transplantation is required. We aimed to characterise this progression by performing single nuclei transcriptomic analysis of liver biopsies taken from patients across the disease spectrum. We have observed that hepatocytes are the cell type affected mostly by the disease and describe plasticity between cell types which may represent a regenerative process.

2024-04-04 | GSE202379 | GEO

Effects of NAFLD/NASH on hepatic gene expression.

2014-01-03 | GSE53381 | GEO

Dyslipidemia Alters HDL Metabolism and Function in NAFLD

Project description:Dyslipidemia and inflammation play key roles in the pathogenesis of both nonalcoholic fatty liver disease (NAFLD) and atherosclerosis. NAFLD, particularly its severe form nonalcoholic steatohepatitis (NASH) is associated with increased cardiovascular disease (CVD) risk. HDL (high density lipoprotein- also a CVD risk) are decreased in NAFLD but whether HDL function is abnormal in NAFLD is unknown. Furthermore, it is unknown whether dyslipidemia contributes to reduced HDL function in NAFLD and whether hepatic inflammation further impairs HDL function in patients with NASH. Therefore, the aim of this study was to investigate HDL function and to examine the effect of dyslipidemia and inflammation on HDL metabolism in patients with biopsy-proven simple steatosis (SS) and NASH. RESULTS: Compared to controls, SS and NASH subjects had significantly higher levels of plasma triglyceride, insulin, and were more insulin resistant (HOMA, P<0.05) with no differences in total cholesterol, HDL cholesterol, ApoB100 and ApoAI levels. NAFLD patients had increased production and degradation rates of both HDLc and ApoAI that resulted in their levels remaining stable. The degradation rates also were increased of other HDL proteins, including ApoAII, ApoAIV, vitamin D-binding protein, and complement 3 (all P<0.05). NAFLD patients had increased activities of LCAT and CETP, indicating altered HDL lipidation. NAFLD induced alterations in HDL metabolism were associated with reduced anti-oxidant but increased pro-inflammatory activity of HDL. However, no differences were observed in either HDL function or the kinetics of HDLc and HDL proteins between SS and NASH subjects.

2019-08-12 | PXD010199 | Pride

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