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EXNADMINA

EXercise as a regulator of hepatic NAD metabolism and MItochondrial function in Non-Alcoholic fatty liver disease

Total Cost €

EC-Contrib. €

Partnership

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Outcomes and
results

EXNADMINA project word cloud

Explore the words cloud of the EXNADMINA project. It provides you a very rough idea of what is the project "EXNADMINA" about.

lipid levels effect approved pathogenic showed therapeutic muscle fibrosis exercise mechanism accumulation interaction examine dependent nad alcoholic nash lack physical maintenance nafld skeletal pool treatment disorders exert mediated countries nicotinamide first hepatic combining function supervisor metabolism ing fatty besides non spectrum steatosis prevalent progression steatohepatitis prevention models inflammation hepatocytes implicated enzymes ultimately positive ranging clear options fellow restoration life industrialized dinucleotide incompletely liver dysfunction organellar dysregulated comprehensively adenine style expertise mitochondrial mouse hypothesize prevent disease action

Project "EXNADMINA" data sheet

The following table provides information about the project.

Coordinator	THE UNIVERSITY OF BIRMINGHAM Organization address address: Edgbaston city: BIRMINGHAM postcode: B15 2TT website: www.bham.ac.uk contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.
Coordinator Country	United Kingdom [UK]
Project website	https://www.birmingham.ac.uk/staff/profiles/metabolism-systems/Lavery-Gareth.aspx
Total cost	146˙591 €
EC max contribution	146˙591 € (100%)
Programme	1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
Code Call	H2020-MSCA-IF-2015
Funding Scheme	MSCA-IF-EF-ST
Starting year	2016
Duration (year-month-day)	from 2016-09-01 to 2018-02-28

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	THE UNIVERSITY OF BIRMINGHAM THE UNIVERSITY OF BIRMINGHAM Organization address address: Edgbaston city: BIRMINGHAM postcode: B15 2TT website: www.bham.ac.uk contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	UK (BIRMINGHAM)	coordinator	146˙591.00

Map

Project objective

Non-alcoholic fatty liver disease (NAFLD) has become the most prevalent liver disease in industrialized countries, including Europe, and comprises a spectrum of disorders ranging from hepatic lipid accumulation (steatosis) to inflammation (non-alcoholic steatohepatitis, NASH) and fibrosis. Pathogenic pathways leading from hepatic steatosis to NASH are still incompletely understood resulting in a lack of approved therapeutic options besides life style changes. Physical activity is effective to prevent NAFLD progression. The mechanism of exercise action on liver mitochondrial metabolism is not clear yet. However, exercise might exert its positive effects via increasing hepatic nicotinamide adenine dinucleotide (NAD) levels. Several studies showed that the hepatic NAD metabolism is dysregulated during the development of NAFLD and that exercise has a positive effect on NAD metabolism and function of NAD dependent enzymes in skeletal muscle. The functionality of mitochondrial metabolism is highly dependent on the maintenance of the organellar NAD pool. Mitochondrial dysfunction has been implicated in the progression from steatosis to NASH. We hypothesize that a dysregulated NAD metabolism in the liver is involved in the development of hepatic mitochondrial dysfunction in NAFLD/NASH. Our overall aim is to define the impact of exercise on hepatic mitochondrial dysfunction and test whether exercise effects are mediated via restoration of NAD metabolism. We will achieve this by combining the knowledge on hepatic NAD metabolism of the fellow with the expertise in exercise mouse models and on analysis of mitochondrial function of the Supervisor. This study is one of the first to comprehensively examine the interaction between exercise, mitochondrial dysfunction as a cause of NAFLD and NAD metabolism specifically in the liver and in hepatocytes and ultimately aims to identify novel therapeutic targets for the prevention and treatment of NAFLD.

Publications

List of publications.
year	authors and title	journal	last update
2017	Rachel S. Fletcher, Joanna Ratajczak, Craig L. Doig, Lucy A. Oakey, Rebecca Callingham, Gabriella Da Silva Xavier, Antje Garten, Yasir S. Elhassan, Philip Redpath, Marie E. Migaud, Andrew Philp, Charles Brenner, Carles Canto, Gareth G. Lavery Nicotinamide riboside kinases display redundancy in mediating nicotinamide mononucleotide and nicotinamide riboside metabolism in skeletal muscle cells published pages: 819-832, ISSN: 2212-8778, DOI: 10.1016/j.molmet.2017.05.011	Molecular Metabolism 6/8	2019-06-13

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