Literature DB >> 26639393

Model-guided identification of a therapeutic strategy to reduce hyperammonemia in liver diseases.

Ahmed Ghallab1, Géraldine Cellière2, Sebastian G Henkel3, Dominik Driesch3, Stefan Hoehme4, Ute Hofmann5, Sebastian Zellmer6, Patricio Godoy7, Agapios Sachinidis8, Meinolf Blaszkewicz7, Raymond Reif7, Rosemarie Marchan7, Lars Kuepfer9, Dieter Häussinger10, Dirk Drasdo11, Rolf Gebhardt6, Jan G Hengstler12.   

Abstract

BACKGROUND & AIMS: Recently, spatial-temporal/metabolic mathematical models have been established that allow the simulation of metabolic processes in tissues. We applied these models to decipher ammonia detoxification mechanisms in the liver.
METHODS: An integrated metabolic-spatial-temporal model was used to generate hypotheses of ammonia metabolism. Predicted mechanisms were validated using time-resolved analyses of nitrogen metabolism, activity analyses, immunostaining and gene expression after induction of liver damage in mice. Moreover, blood from the portal vein, liver vein and mixed venous blood was analyzed in a time dependent manner.
RESULTS: Modeling revealed an underestimation of ammonia consumption after liver damage when only the currently established mechanisms of ammonia detoxification were simulated. By iterative cycles of modeling and experiments, the reductive amidation of alpha-ketoglutarate (α-KG) via glutamate dehydrogenase (GDH) was identified as the lacking component. GDH is released from damaged hepatocytes into the blood where it consumes ammonia to generate glutamate, thereby providing systemic protection against hyperammonemia. This mechanism was exploited therapeutically in a mouse model of hyperammonemia by injecting GDH together with optimized doses of cofactors. Intravenous injection of GDH (720 U/kg), α-KG (280 mg/kg) and NADPH (180 mg/kg) reduced the elevated blood ammonia concentrations (>200 μM) to levels close to normal within only 15 min.
CONCLUSION: If successfully translated to patients the GDH-based therapy might provide a less aggressive therapeutic alternative for patients with severe hyperammonemia.
Copyright © 2015 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Ammonia; Liver damage; Liver regeneration; Spatio-temporal model; Systems biology

Mesh:

Substances:

Year:  2015        PMID: 26639393     DOI: 10.1016/j.jhep.2015.11.018

Source DB:  PubMed          Journal:  J Hepatol        ISSN: 0168-8278            Impact factor:   25.083


  32 in total

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