Transcriptomic analysis of liver mRNA from TSP-1 KO and WT mice fed with normal diet or choline deficient amino acid defined diet (CDAHFD, human NASH model)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA495159 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptomic profiles of wild type and TSP1 knockout mice that were fed control (normal) diet or CDAHFD (choline deficient amino acid defiend high fat diet) chow for 12 weeks to model Non-alcoholic Steatohepatitis (NASH) disease in humans.
2019-05-31 | GSE120977 | GEO
Project description:Nonalcoholic Fatty Liver Disease (NAFLD) is a broad spectrum of liver disorders ranging from simple steatosis to nonalcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. The choline-deficient L-amino acid-defined (CDAA) diet-induced NAFLD animal model has traditionally been used to understand the molecular mechanisms of disease development and progression. Although this animal model shows a similar course of disease progression to human NAFLD, it does not develop comorbidities such as obesity and type 2 diabetes. Therefore, its relevance to human NAFLD (what aspects of the disease etiology are recapitulated in this model?) is not fully understood. We applied microarray analysis to characterize its pathophysiology, and evaluate the similarity across species.
2023-03-25 | GSE227714 | GEO
Project description:Non-alcoholic steatohepatitis (NASH) is the most significant cause of chronic liver disease worldwide, with limited therapeutic options. In this experiment, a choline-deficient amino acid-defined high fat diet (CDAHFD) were used to construct a mouse NASH model. After 16 weeks of CDAHFD diets, liver samples were collected. We want to further confirm that the elevated EFHD2 is specifically expressed in infiltrated macrophages/monocytes in NASH.
2024-01-01 | GSE243079 | GEO
Project description:To investigate the role of hepatic CYP2B in diet-induced nonalcoholic steatohepatitis (NASH), a Cyp2b triple knockout mouse lacking Cyp2b9, Cyp2b10, and Cyp2b13 was developed using CRISPER/Cas9. Wildtype (WT) and Cyp2b-null mice were fed a normal diet (ND) or a choline-deficient, L-amino acid-defined high-fat diet (CDAHFD), containing 0.1% methionine and 62% fat for 8 weeks. RNA was extracted from the livers of female and male mice from all treatment groups and used for RNA seqencing. RNAseq data demonstrated that a lack of Cyp2b was protective in female but more harmful in male mice. Hepatic gene expression revealed a higher number of phase I-III xenobiotic metabolism and inflammatory response genes were down-regulated in CDAHFD-fed WT female and Cyp2b-null male mice.
2019-12-31 | GSE137449 | GEO
Project description:The objective of this study was to identify metabolic regulatory mechanisms affected by choline availability in rainbow trout (Oncorhynchus mykiss) broodstock diets associated with increased offspring growth performance. Three customized diets were formulated to have different levels of choline: (a) 0% choline supplementation (Low Choline: 2065 ppm choline), (b) 0.6% choline supplementation (Medium Choline: 5657 ppm choline), and (c) 1.2% choline supplementation (High Choline: 9248 ppm choline). Six all-female rainbow trout families were fed experimental diets beginning 18 months post-hatch until spawning; their offspring were fed a commercial diet. Experimental broodstock diet did not affect overall choline, fatty acid, or amino acid content in the oocytes (p > 0.05), apart from tyrosine (p ≤ 0.05). Offspring body weights from the High and Low Choline diets did not differ from those in the Medium Choline diet (p > 0.05); however, family-by-diet and sire-by-diet interactions on offspring growth were detected (p ≤ 0.05). The High Choline diet did not improve growth performance in the six broodstock families at final harvest (520-days post-hatch, or dph). Numerous genes associated with muscle development and lipid metabolism were identified, including myosin, troponin C, and fatty acid binding proteins, which were associated with key signaling pathways of lipid metabolism, muscle cell development, muscle cell proliferation, and muscle cell differentiation. These findings indicate that supplementing broodstock diets with choline does regulate expression of genes related to growth and nutrient partitioning but does not lead to growth benefits in rainbow trout families selected for disease resistance.
2024-02-09 | GSE243186 | GEO
Project description:Recent studies have revealed the pivotal role of gut microbiota in the precession of liver diseases including non-alcoholic steatohepatitis (NASH). Many natural herbs, such as Gynostemma pentaphyllum (GP), have been extensively used applied in the treatment prevention of NASH, while the bioactive components and underlying mechanism remain unclear. The aim of this study was to investigate whether the polysaccharides of GP (GPP) has the protective effect on of NASH and to explore the potential mechanism underlying these effects. To investigate the function high dose of GPP(HGPP) in the regulation of hepatic gene expression, C57BL/6 male mice were fed with methionine-choline-deficient (MCD) diet for 4 weeks to induce NASH, and administered daily oral gavage of the sodium carboxymethylcellulose (CMC-Na) for model group, HGPP for experimental group, compared with normal control methionine-choline-sufficient (MCS) group.
2022-06-16 | GSE205974 | GEO
Project description:The objective of this study is to explore gene expression profiles of liver tissues in response to choline defficient diet by DNA microarray data analysis. Male CD-1mice (5 weeks) were fed either a choline-deficient diet (F2CDD, Oriental Yeast) or F2CDD plus 0.2% choline bitartrate for 3 weeks. Liver tissue from control versus choline-deficient samples were analyzed for gene expression on an Agilent Whole Mouse Genome Microarray.
2016-02-25 | E-GEOD-78053 | biostudies-arrayexpress
Project description:Non-alcoholic steatohepatitis (NASH) is becoming one of the leading causes of hepatocellular carcinoma (HCC), replacing viral HBV-, HCV-, and alcohol-related chronic liver diseases as major etiological risk of factors for HCC. The goal of the present study was to investigate transcriptomic alterations in the livers of male C57BL/6J mice fed a choline- and folate-deficient (CFD) diet. Feeding mice a CFD diet for 12 weeks caused NASH-like liver injury exhibiting uniform morphological features of human NASH. High-throughput whole-genome transcriptomic analysis showed that 1750 genes were differentially expressed (344 down-regulated and 1396 up-regulated) in the livers of mice fed a CFD diet as compared to control mice. The functional pathway analysis revealed that these differentially-expressed genes were associated with diverse cellular processes, including cellular growth and differentiation, cell-to-cell signaling and interaction, lipid metabolism, inflammation, fibrosis, molecular transport, and drug metabolism. These findings demonstrate that deregulation of global gene expression is the prominent fundamental feature of NASH in mice induced by a CFD diet.
2017-03-23 | GSE96936 | GEO
Project description:Nonalcoholic steatohepatitis (NASH) is a major cause of liver fibrosis with increasing prevalence worldwide. Currently there are no approved drugs available. The development of new therapies is difficult as diagnosis and staging requires biopsies. Consequently, predictive plasma biomarkers would be useful for drug development. To identify new plasma biomarkers in a choline-deficient L-amino acid-defined diet rat NASH model we analyzed liver and plasma samples by proteomics, revealing disease relevant signatures and a high correlation between liver mRNA and protein changes. We developed a multi-dimensional attribute ranking approach integrating multi-omics data with liver histology and prior knowledge uncovering known human markers, but also novel candidates. Using regression analysis, we show that the top-ranked plasma markers were highly predictive for fibrosis in our model and hence can serve as preclinical plasma biomarkers. Our approach presented here illustrates the power of multi-omics analyses combined with plasma proteomics and is readily applicable to human biomarker discovery.
2020-01-28 | PXD014751 | Pride
Project description:Kupffer cells (KCs) self-renew by local proliferation in the adult independently from monocytes (Mos). However, how they maintain during chronic metabolic disorders such as non-alcoholic steatohepatitis (NASH) remains ill-defined. We characterized KCs during NASH and observed diversity in the KC pool, with a significant fraction of monocyte-derived KCs (MoKCs). Here, we aim to uncover the transcriptional landscapes of KCs subsets found in a mouse model of methionine and choline deficient (MCD)-diet induced non-alcoholic steatohepatitis (NASH).
2020-12-04 | GSE138778 | GEO