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

Zugehörigkeit
Institute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany.
Berndt, Nikolaus;
Zugehörigkeit
Institute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany.
Bulik, Sascha;
Zugehörigkeit
Institute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany.
Wallach, Iwona;
Zugehörigkeit
Department of General, Visceral and Transplantation Surgery Augustenburger Platz, Charité - Universitätsmedizin Berlin - Campus Virchow-Klinikum, 113353, Berlin, Germany.
Wünsch, Tilo;
ORCID
0000-0003-1725-179X
Zugehörigkeit
Institute for Biology, Institute for Theoretical Biology, Humboldt-University Berlin, Invalidenstraße 43, Haus, 410115, Berlin, Germany.
König, Matthias;
Zugehörigkeit
German Federal Institute for Risk Assessment Max-Dohrn-Straße 8-10, 10589, Berlin, Germany.
Stockmann, Martin;
ORCID
0000-0002-0170-868X
Zugehörigkeit
Max Planck Institute of Molecular Genetics/Mass Spectroscopy, Ihnestraße 63-73, 14195, Berlin, Germany.
Meierhofer, David;
Zugehörigkeit
Institute of Biochemistry Computational Systems Biochemistry Group, Charité - Universitätsmedizin Berlin, Charitéplatz, 110117, Berlin, Germany. hergo@charite.de.
Holzhütter, Hermann-Georg

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).

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