NASH LiverModel transcriptome
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE224645 | GEO | 2025/03/19
REPOSITORIES: GEO
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Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays
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Project description:Non-alcoholic fatty liver disease (NAFLD) encompasses a spectrum of disease that ranges from simple steatosis, to inflammatory form non-alcoholic steatohepatitis (NASH), cirrhosis, and up to hepatocellular carcinoma. While NASH usually takes decades to develop at a rate of one stage per seven years, in the case of post-trasplant NASH (pt-NASH) develops fibrosis much more rapidly, with almost 50% of liver transplant recipients presenting stage 3 fibrosis by 5 years post-transplant. Archived fresh-frozen transplanted liver biopsy samples from four liver biopsy samples with evidence of NASH (2 recurrent and 2 de novo), two with simple steatosis (both de novo), and five with normal histology as controls had their transcriptome sequenced in two batches for deeper coverage.
2022-05-09 | E-MTAB-11688 | biostudies-arrayexpress
Project description:Non-alcoholic fatty liver disease (NAFLD) is a consequence of sedentary life style and high fat diets with an estimated prevalence of about 30% in western countries. It is associated with insulin resistance, obesity, glucose intolerance and drug toxicity. Additionally, polymorphisms in, e.g. APOC3, PNPLA3, NCAN and PPP1R3B, correlate with NAFLD. Several studies have already investigated later stages of the disease. This study characterizes and stratifies distinct grades of the early steatosis stages of the disease with the aim of identifying mechanisms underlying the etiology of the disease. We analyzed liver biopsies and serum samples from patients with distinct grades of steatosis (also pre-disease states) employing transcriptomics, serum biomarkers, metabolomics, and proteomics. We unveiled distinct transcriptome, proteome and metabolome profiles in patients with high-grade and low-grade steatosis. In line with previously reported causes of steatosis and insulin resistance our observed expression differences in the levels of cytokines, in the IGF-axis, in fat metabolism and branched chain amino acids provide a comprehensive image of the deregulated biological system underlying the disease.
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Project description:The liver is undergoing major rearrangements during the development of non-alcoholic steatohepatitis (NASH), from steatosis to severe lipid accumulation, inflammation and fibrosis. The mechanisms for this transition and the molecular changes preceding NASH are not fully understood. Here, we perform a single-cell RNA sequencing survey of 13,240 mouse liver cells during the development of non-alcoholic fatty liver disease. By measuring the entire transcriptome on a single-cell level from mice in the early stages of NASH development, we recognize known hepatocyte cell populations, Kupffer cells and stellate cells, as well as distinct gene expression changes in hepatocytes. We also reveal high hepatocyte heterogeneity in steatosis markers which projects a lipogenic trajectory of known and novel steatosis-associated genes. Importantly, we uncover distinct clusters of hepatocytes characterized by high or low Srebp1c expression with unique molecular signatures of lipogenesis. These results identify a novel regulatory pathway for lipogenesis in the liver that contributes to NASH progression.
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