Rattus norvegicus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA273424 | ENA |
REPOSITORIES: ENA
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2015-01-23 | E-GEOD-65220 | biostudies-arrayexpress
Project description:Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with NAFLD and its progression. Microarrays were used to identify hepatic gene expression changes in each of these models. The goal is to identify a predictor of different NAFLD progressions. Non-alcoholic fatty liver disease (NAFLD) is recognized as a low-grade systemic inflammatory state with both hepatic and extra-hepatic manifestations. We aimed to identify common key regulators and adaptive pathways in different NAFLD phenotypes. NAFL, NASH and NAFL+T2DM rat models were used to represent simple fatty liver, fatty liver with severe hepatic manifestations, and fatty liver with severe metabolic manifestations, respectively. We applied microarray analysis to characterize the key regulators and adaptive pathways in different NAFLD phenotypes.
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Project description:Non-alcoholic Steatohepatitis following feeding of high polyunsaturated fat diets
| PRJNA101201 | ENA
Project description:Global gene expression patterns of 2 human steatosis and 9 human non-alcoholic steatohepatitis (NASH) together with their respective control patterns were analyzed to define the non-alcoholic fatty liver disease (NAFLD) progression molecular characteristics and to define NASH early markers from steatosis. Human liver samples of steatosis and non-alcoholic steatohepatitis were selected for RNA extraction and hybridization on Affymetrix microarrays. This dataset is part of the TransQST collection.
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Project description:Mardinoglu2014 - Genome-scale metabolic model
(HMR version 2.0) - human hepatocytes (iHepatocytes2322)
This model is described in the article:
Genome-scale metabolic
modelling of hepatocytes reveals serine deficiency in patients
with non-alcoholic fatty liver disease.
Mardinoglu A, Agren R, Kampf C,
Asplund A, Uhlen M, Nielsen J.
Nat Commun 2014; 5: 3083
Abstract:
Several liver disorders result from perturbations in the
metabolism of hepatocytes, and their underlying mechanisms can
be outlined through the use of genome-scale metabolic models
(GEMs). Here we reconstruct a consensus GEM for hepatocytes,
which we call iHepatocytes2322, that extends previous models by
including an extensive description of lipid metabolism. We
build iHepatocytes2322 using Human Metabolic Reaction 2.0
database and proteomics data in Human Protein Atlas, which
experimentally validates the incorporated reactions. The
reconstruction process enables improved annotation of the
proteomics data using the network centric view of
iHepatocytes2322. We then use iHepatocytes2322 to analyse
transcriptomics data obtained from patients with non-alcoholic
fatty liver disease. We show that blood concentrations of
chondroitin and heparan sulphates are suitable for diagnosing
non-alcoholic steatohepatitis and for the staging of
non-alcoholic fatty liver disease. Furthermore, we observe
serine deficiency in patients with NASH and identify PSPH,
SHMT1 and BCAT1 as potential therapeutic targets for the
treatment of non-alcoholic steatohepatitis.
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MODEL1402200003.
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2005-01-01 | MODEL1402200003 | BioModels
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