Evidence map›Paper›PMID 29921957›Full record

ArticleNature communications2018

HEPATOKIN1 is a biochemistry-based model of liver metabolism for applications in medicine and pharmacology.

Nikolaus Berndt, Sascha Bulik, Iwona Wallach, Tilo Wünsch, Matthias König, Martin Stockmann, David Meierhofer, Hermann-Georg Holzhütter

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.5field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

34 citing papers in PubMed, 72 citations in OpenAlex.

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  14. Kinetic Modeling of Hepatic Metabolism and Simulation of Treatment Effects.Methods in molecular biology (Clifton, N.J.) · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

Nikolaus BerndtInstitute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany.
Sascha BulikInstitute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany.
Iwona WallachInstitute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany.
Tilo WünschDepartment of General, Visceral and Transplantation Surgery Augustenburger Platz, Charité - Universitätsmedizin Berlin - Campus Virchow-Klinikum, 113353, Berlin, Germany.
Matthias KönigInstitute for Biology, Institute for Theoretical Biology, Humboldt-University Berlin, Invalidenstraße 43, Haus, 410115, Berlin, Germany.ORCID http://orcid.org/0000-0003-1725-179X
Martin StockmannGerman Federal Institute for Risk Assessment Max-Dohrn-Straße 8-10, 10589, Berlin, Germany.
David MeierhoferMax Planck Institute of Molecular Genetics/Mass Spectroscopy, Ihnestraße 63-73, 14195, Berlin, Germany.ORCID http://orcid.org/0000-0002-0170-868X
Hermann-Georg HolzhütterInstitute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany. hergo@charite.de.
Charité - Universitätsmedizin Berlin · DEFederal Institute for Risk Assessment · DEHumboldt-Universität zu Berlin · DEMax Planck Institute for Molecular Genetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The epidemic increase of non-alcoholic fatty liver diseases (NAFLD) requires a deeper understanding of the regulatory circuits controlling the response of liver metabolism to nutritional challenges, medical drugs, and genetic enzyme variants. As in vivo studies of human liver metabolism are encumbered with serious ethical and technical issues, we developed a comprehensive biochemistry-based kinetic model of the central liver metabolism including the regulation of enzyme activities by their reactants, allosteric effectors, and hormone-dependent phosphorylation. The utility of the model for basic research and applications in medicine and pharmacology is illustrated by simulating diurnal variations of the metabolic state of the liver at various perturbations caused by nutritional challenges (alcohol), drugs (valproate), and inherited enzyme disorders (galactosemia). Using proteomics data to scale maximal enzyme activities, the model is used to highlight differences in the metabolic functions of normal hepatocytes and malignant liver cells (adenoma and hepatocellular carcinoma).

Indexed as

AlgorithmsMetabolic Networks and PathwaysModels, BiologicalCarcinoma, HepatocellularEnzyme InhibitorsGalactosemiasHepatocytesHumansKineticsLiverLiver NeoplasmsNon-alcoholic Fatty Liver DiseaseProteomicsValproic AcidEnzyme InhibitorsValproic Acid

Identifiers

PMID29921957
PMCPMC6008457
OpenAlexW2808180679

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.