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MODEL1402200003 - Mardinoglu2014 - Genome-scale metabolic model (HMR version 2.0) - human hepatocytes (iHepatocytes2322)


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Reference Publication
Publication ID: 24419221
Mardinoglu A, Agren R, Kampf C, Asplund A, Uhlen M, Nielsen J.
Genome-scale metabolic modelling of hepatocytes reveals serine deficiency in patients with non-alcoholic fatty liver disease.
Nat Commun 2014; 5: 3083
1] Department of Chemical and Biological Engineering, Chalmers University of Technology, Kamivangen 10, Gothenburg SE-412 96, Sweden [2].  [more]
Original Model: Human Metabolic Reaction (...
Submitter: Adil Mardinoglu
Submission Date: 20 Feb 2014 10:37:23 UTC
Last Modification Date: 18 Aug 2017 15:14:56 UTC
Creation Date: 01 Feb 2014 18:35:23 UTC
Non kinetic model: network icon.
Encoders:  Adil Mardinoglu
bqmodel:isDerivedFrom PubMed 17882155
PubMed 17267599
PubMed 20823849
bqbiol:occursIn Brenda Tissue Ontology hepatocyte
bqbiol:hasTaxon Taxonomy Homo sapiens
bqbiol:isVersionOf Gene Ontology cellular metabolic process
Mardinoglu2014 - Genome-scale metabolic model (HMR version 2.0) - human hepatocytes (iHepatocytes2322)

This model is described in the article:

Mardinoglu A, Agren R, Kampf C, Asplund A, Uhlen M, Nielsen J.
Nat Commun 2014; 5: 3083


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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