ArticleCell reports2016
In Silico Modeling of Liver Metabolism in a Human Disease Reveals a Key Enzyme for Histidine and Histamine Homeostasis.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 34 citations in OpenAlex.
- DietaryFrontiers in microbiology · 2026Article
- Tolerance to NADH/NADiScience · 2021Article
- Fat Induces Glucose Metabolism in Nontransformed Liver Cells and Promotes Liver Tumorigenesis.Cancer research · 2021Article
- Metabolic Reprogramming and Reconstruction: Integration of Experimental and Computational Studies to Set the Path Forward in ADPKD.Frontiers in medicine · 2021Review
- Fibroblast-specific genome-scale modelling predicts an imbalance in amino acid metabolism in Refsum disease.The FEBS journal · 2020Article
- Genetic buffering and potentiation in metabolism.PLoS computational biology · 2020Article
- Opportunities at the Interface of Network Science and Metabolic Modeling.Frontiers in bioengineering and biotechnology · 2020Review
- Metabolic rearrangements in primary liver cancers: cause and consequences.Nature reviews. Gastroenterology & hepatology · 2019Review
- Human Systems Biology and Metabolic Modelling: A Review-From Disease Metabolism to Precision Medicine.BioMed research international · 2019Review
- Flux-dependent graphs for metabolic networks.NPJ systems biology and applications · 2018Article
- Dissection of metabolic reprogramming in polycystic kidney disease reveals coordinated rewiring of bioenergetic pathways.Communications biology · 2018Article
- Quantitative systems pharmacology and the personalized drug-microbiota-diet axis.Current opinion in systems biology · 2017Review
- Computational Modeling in Liver Surgery.Frontiers in physiology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Primary hyperoxaluria type I (PH1) is an autosomal-recessive inborn error of liver metabolism caused by alanine:glyoxylate aminotransferase (AGT) deficiency. In silico modeling of liver metabolism in PH1 recapitulated accumulation of known biomarkers as well as alteration of histidine and histamine levels, which we confirmed in vitro, in vivo, and in PH1 patients. AGT-deficient mice showed decreased vascular permeability, a readout of in vivo histamine activity. Histamine reduction is most likely caused by increased catabolism of the histamine precursor histidine, triggered by rerouting of alanine flux from AGT to the glutamic-pyruvate transaminase (GPT, also known as the alanine-transaminase ALT). Alanine administration reduces histamine levels in wild-type mice, while overexpression of GPT in PH1 mice increases plasma histidine, normalizes histamine levels, restores vascular permeability, and decreases urinary oxalate levels. Our work demonstrates that genome-scale metabolic models are clinically relevant and can link genotype to phenotype in metabolic disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.