AustralieFrV1, Ncbi, Merge, bibRecord, 004396

Personal model-assisted identification of NAD(+) and glutathione metabolism as intervention target in NAFLD.

Identifieur interne : 004396 ( Ncbi/Merge ); précédent : 004395; suivant : 004397

Personal model-assisted identification of NAD(+) and glutathione metabolism as intervention target in NAFLD.

Auteurs : Adil Mardinoglu [Suède] ; Elias Bjornson [Suède] ; Cheng Zhang [Suède] ; Martina Klevstig [Suède] ; Sanni Söderlund [Finlande] ; Marcus St Hlman [Suède] ; Martin Adiels [Suède] ; Antti Hakkarainen [Finlande] ; Nina Lundbom [Finlande] ; Murat Kilicarslan [Pays-Bas] ; Björn M. Hallström [Suède] ; Jesper Lundbom [Finlande] ; Bruno Vergès [France] ; Peter Hugh R. Barrett [Australie] ; Gerald F. Watts [Australie] ; Mireille J. Serlie [Pays-Bas] ; Jens Nielsen [Suède] ; Mathias Uhlén [Suède] ; Ulf Smith [Suède] ; Hanns-Ulrich Marschall [Suède] ; Marja-Riitta Taskinen [Finlande] ; Jan Boren [Suède]

Source :

Molecular systems biology [ 1744-4292 ] ; 2017.

RBID : pubmed:28254760

Descripteurs français

KwdFr :
- Adulte d'âge moyen, Animaux, Femelle, Foie (enzymologie), Foie (métabolisme), Glutathion (métabolisme), Glycine (sang), Génome, Humains, Lipoprotéines (métabolisme), Modèles animaux de maladie humaine, Modélisation spécifique au patient, Mâle, Métabolomique (), NAD (métabolisme), Régulation de l'expression des gènes codant pour des enzymes, Souris, Stéatose hépatique non alcoolique (diétothérapie), Stéatose hépatique non alcoolique (génétique), Stéatose hépatique non alcoolique (métabolisme), Sérine (administration et posologie), Sérine (sang), Sérine (usage thérapeutique).
MESH :
- administration et posologie : Sérine.
- diétothérapie : Stéatose hépatique non alcoolique.
- enzymologie : Foie.
- génétique : Stéatose hépatique non alcoolique.
- métabolisme : Foie, Glutathion, Lipoprotéines, NAD, Stéatose hépatique non alcoolique.
- sang : Glycine, Sérine.
- usage thérapeutique : Sérine.
- Adulte d'âge moyen, Animaux, Femelle, Génome, Humains, Modèles animaux de maladie humaine, Modélisation spécifique au patient, Mâle, Métabolomique, Régulation de l'expression des gènes codant pour des enzymes, Souris.

English descriptors

KwdEn :
- Animals, Disease Models, Animal, Female, Gene Expression Regulation, Enzymologic, Genome, Glutathione (metabolism), Glycine (blood), Humans, Lipoproteins (metabolism), Liver (enzymology), Liver (metabolism), Male, Metabolomics (methods), Mice, Middle Aged, NAD (metabolism), Non-alcoholic Fatty Liver Disease (diet therapy), Non-alcoholic Fatty Liver Disease (genetics), Non-alcoholic Fatty Liver Disease (metabolism), Patient-Specific Modeling, Serine (administration & dosage), Serine (blood), Serine (therapeutic use).
MESH :
- chemical , administration & dosage : Serine.
- chemical , blood : Glycine, Serine.
- chemical , metabolism : Glutathione, Lipoproteins, NAD.
- diet therapy : Non-alcoholic Fatty Liver Disease.
- enzymology : Liver.
- genetics : Non-alcoholic Fatty Liver Disease.
- metabolism : Liver, Non-alcoholic Fatty Liver Disease.
- methods : Metabolomics.
- chemical , therapeutic use : Serine.
- Animals, Disease Models, Animal, Female, Gene Expression Regulation, Enzymologic, Genome, Humans, Male, Mice, Middle Aged, Patient-Specific Modeling.

Abstract

To elucidate the molecular mechanisms underlying non-alcoholic fatty liver disease (NAFLD), we recruited 86 subjects with varying degrees of hepatic steatosis (HS). We obtained experimental data on lipoprotein fluxes and used these individual measurements as personalized constraints of a hepatocyte genome-scale metabolic model to investigate metabolic differences in liver, taking into account its interactions with other tissues. Our systems level analysis predicted an altered demand for NAD(+) and glutathione (GSH) in subjects with high HS Our analysis and metabolomic measurements showed that plasma levels of glycine, serine, and associated metabolites are negatively correlated with HS, suggesting that these GSH metabolism precursors might be limiting. Quantification of the hepatic expression levels of the associated enzymes further pointed to altered de novo GSH synthesis. To assess the effect of GSH and NAD(+) repletion on the development of NAFLD, we added precursors for GSH and NAD(+) biosynthesis to the Western diet and demonstrated that supplementation prevents HS in mice. In a proof-of-concept human study, we found improved liver function and decreased HS after supplementation with serine (a precursor to glycine) and hereby propose a strategy for NAFLD treatment.

PubMed: 28254760

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to stream PubMed, to step Curation: 001010
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pubmed:28254760

Le document en format XML

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<author><name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F" last="Watts">Gerald F. Watts</name>
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<author><name sortKey="Smith, Ulf" sort="Smith, Ulf" uniqKey="Smith U" first="Ulf" last="Smith">Ulf Smith</name>
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<author><name sortKey="Marschall, Hanns Ulrich" sort="Marschall, Hanns Ulrich" uniqKey="Marschall H" first="Hanns-Ulrich" last="Marschall">Hanns-Ulrich Marschall</name>
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<author><name sortKey="Taskinen, Marja Riitta" sort="Taskinen, Marja Riitta" uniqKey="Taskinen M" first="Marja-Riitta" last="Taskinen">Marja-Riitta Taskinen</name>
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<country xml:lang="fr">Finlande</country>
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<author><name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Boren">Jan Boren</name>
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<country wicri:rule="url">Suède</country>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Personal model-assisted identification of NAD(+) and glutathione metabolism as intervention target in NAFLD.</title>
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<author><name sortKey="Bjornson, Elias" sort="Bjornson, Elias" uniqKey="Bjornson E" first="Elias" last="Bjornson">Elias Bjornson</name>
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<country xml:lang="fr">Suède</country>
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<author><name sortKey="Zhang, Cheng" sort="Zhang, Cheng" uniqKey="Zhang C" first="Cheng" last="Zhang">Cheng Zhang</name>
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<author><name sortKey="Klevstig, Martina" sort="Klevstig, Martina" uniqKey="Klevstig M" first="Martina" last="Klevstig">Martina Klevstig</name>
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<author><name sortKey="Soderlund, Sanni" sort="Soderlund, Sanni" uniqKey="Soderlund S" first="Sanni" last="Söderlund">Sanni Söderlund</name>
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<author><name sortKey="St Hlman, Marcus" sort="St Hlman, Marcus" uniqKey="St Hlman M" first="Marcus" last="St Hlman">Marcus St Hlman</name>
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<author><name sortKey="Adiels, Martin" sort="Adiels, Martin" uniqKey="Adiels M" first="Martin" last="Adiels">Martin Adiels</name>
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<wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg</wicri:regionArea>
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<author><name sortKey="Hakkarainen, Antti" sort="Hakkarainen, Antti" uniqKey="Hakkarainen A" first="Antti" last="Hakkarainen">Antti Hakkarainen</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.</nlm:affiliation>
<country xml:lang="fr">Finlande</country>
<wicri:regionArea>Department of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki</wicri:regionArea>
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</affiliation>
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<author><name sortKey="Lundbom, Nina" sort="Lundbom, Nina" uniqKey="Lundbom N" first="Nina" last="Lundbom">Nina Lundbom</name>
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<author><name sortKey="Kilicarslan, Murat" sort="Kilicarslan, Murat" uniqKey="Kilicarslan M" first="Murat" last="Kilicarslan">Murat Kilicarslan</name>
<affiliation wicri:level="4"><nlm:affiliation>Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam</wicri:regionArea>
<placeName><settlement type="city">Amsterdam</settlement>
<region nuts="2" type="province">Hollande-Septentrionale</region>
<settlement type="city">Amsterdam</settlement>
</placeName>
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</author>
<author><name sortKey="Hallstrom, Bjorn M" sort="Hallstrom, Bjorn M" uniqKey="Hallstrom B" first="Björn M" last="Hallström">Björn M. Hallström</name>
<affiliation wicri:level="3"><nlm:affiliation>Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, Sweden.</nlm:affiliation>
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<country xml:lang="fr">Finlande</country>
<wicri:regionArea>Department of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki</wicri:regionArea>
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<author><name sortKey="Verges, Bruno" sort="Verges, Bruno" uniqKey="Verges B" first="Bruno" last="Vergès">Bruno Vergès</name>
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<country xml:lang="fr">France</country>
<wicri:regionArea>Department of Endocrinology-Diabetology, University Hospital and INSERM CRI 866, Dijon</wicri:regionArea>
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<region type="old region">Bourgogne</region>
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<author><name sortKey="Barrett, Peter Hugh R" sort="Barrett, Peter Hugh R" uniqKey="Barrett P" first="Peter Hugh R" last="Barrett">Peter Hugh R. Barrett</name>
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<wicri:regionArea>Faculty of Engineering, Computing and Mathematics, University of Western Australia, Perth, WA</wicri:regionArea>
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<author><name sortKey="Watts, Gerald F" sort="Watts, Gerald F" uniqKey="Watts G" first="Gerald F" last="Watts">Gerald F. Watts</name>
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<country xml:lang="fr">Australie</country>
<wicri:regionArea>Metabolic Research Centre, Cardiovascular Medicine, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, Perth, WA</wicri:regionArea>
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<author><name sortKey="Serlie, Mireille J" sort="Serlie, Mireille J" uniqKey="Serlie M" first="Mireille J" last="Serlie">Mireille J. Serlie</name>
<affiliation wicri:level="4"><nlm:affiliation>Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.</nlm:affiliation>
<country xml:lang="fr">Pays-Bas</country>
<wicri:regionArea>Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam</wicri:regionArea>
<placeName><settlement type="city">Amsterdam</settlement>
<region nuts="2" type="province">Hollande-Septentrionale</region>
<settlement type="city">Amsterdam</settlement>
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<author><name sortKey="Nielsen, Jens" sort="Nielsen, Jens" uniqKey="Nielsen J" first="Jens" last="Nielsen">Jens Nielsen</name>
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<country xml:lang="fr">Suède</country>
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<author><name sortKey="Uhlen, Mathias" sort="Uhlen, Mathias" uniqKey="Uhlen M" first="Mathias" last="Uhlén">Mathias Uhlén</name>
<affiliation wicri:level="3"><nlm:affiliation>Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
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<author><name sortKey="Smith, Ulf" sort="Smith, Ulf" uniqKey="Smith U" first="Ulf" last="Smith">Ulf Smith</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg</wicri:regionArea>
<wicri:noRegion>Gothenburg</wicri:noRegion>
</affiliation>
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<author><name sortKey="Marschall, Hanns Ulrich" sort="Marschall, Hanns Ulrich" uniqKey="Marschall H" first="Hanns-Ulrich" last="Marschall">Hanns-Ulrich Marschall</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.</nlm:affiliation>
<country xml:lang="fr">Suède</country>
<wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg</wicri:regionArea>
<wicri:noRegion>Gothenburg</wicri:noRegion>
</affiliation>
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<author><name sortKey="Taskinen, Marja Riitta" sort="Taskinen, Marja Riitta" uniqKey="Taskinen M" first="Marja-Riitta" last="Taskinen">Marja-Riitta Taskinen</name>
<affiliation wicri:level="1"><nlm:affiliation>Research programs Unit, Diabetes and Obesity, Helsinki University Hospital, University of Helsinki, Helsinki, Finland.</nlm:affiliation>
<country xml:lang="fr">Finlande</country>
<wicri:regionArea>Research programs Unit, Diabetes and Obesity, Helsinki University Hospital, University of Helsinki, Helsinki</wicri:regionArea>
<wicri:noRegion>Helsinki</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Boren, Jan" sort="Boren, Jan" uniqKey="Boren J" first="Jan" last="Boren">Jan Boren</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden adilm@scilifelab.se jan.boren@wlab.gu.se.</nlm:affiliation>
<country wicri:rule="url">Suède</country>
<wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg</wicri:regionArea>
<wicri:noRegion>Gothenburg</wicri:noRegion>
</affiliation>
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<series><title level="j">Molecular systems biology</title>
<idno type="eISSN">1744-4292</idno>
<imprint><date when="2017" type="published">2017</date>
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<term>Disease Models, Animal</term>
<term>Female</term>
<term>Gene Expression Regulation, Enzymologic</term>
<term>Genome</term>
<term>Glutathione (metabolism)</term>
<term>Glycine (blood)</term>
<term>Humans</term>
<term>Lipoproteins (metabolism)</term>
<term>Liver (enzymology)</term>
<term>Liver (metabolism)</term>
<term>Male</term>
<term>Metabolomics (methods)</term>
<term>Mice</term>
<term>Middle Aged</term>
<term>NAD (metabolism)</term>
<term>Non-alcoholic Fatty Liver Disease (diet therapy)</term>
<term>Non-alcoholic Fatty Liver Disease (genetics)</term>
<term>Non-alcoholic Fatty Liver Disease (metabolism)</term>
<term>Patient-Specific Modeling</term>
<term>Serine (administration & dosage)</term>
<term>Serine (blood)</term>
<term>Serine (therapeutic use)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adulte d'âge moyen</term>
<term>Animaux</term>
<term>Femelle</term>
<term>Foie (enzymologie)</term>
<term>Foie (métabolisme)</term>
<term>Glutathion (métabolisme)</term>
<term>Glycine (sang)</term>
<term>Génome</term>
<term>Humains</term>
<term>Lipoprotéines (métabolisme)</term>
<term>Modèles animaux de maladie humaine</term>
<term>Modélisation spécifique au patient</term>
<term>Mâle</term>
<term>Métabolomique ()</term>
<term>NAD (métabolisme)</term>
<term>Régulation de l'expression des gènes codant pour des enzymes</term>
<term>Souris</term>
<term>Stéatose hépatique non alcoolique (diétothérapie)</term>
<term>Stéatose hépatique non alcoolique (génétique)</term>
<term>Stéatose hépatique non alcoolique (métabolisme)</term>
<term>Sérine (administration et posologie)</term>
<term>Sérine (sang)</term>
<term>Sérine (usage thérapeutique)</term>
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<term>Serine</term>
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<term>Lipoproteins</term>
<term>NAD</term>
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</keywords>
<keywords scheme="MESH" qualifier="diet therapy" xml:lang="en"><term>Non-alcoholic Fatty Liver Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="diétothérapie" xml:lang="fr"><term>Stéatose hépatique non alcoolique</term>
</keywords>
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</keywords>
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</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Liver</term>
<term>Non-alcoholic Fatty Liver Disease</term>
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<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Metabolomics</term>
</keywords>
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<term>Glutathion</term>
<term>Lipoprotéines</term>
<term>NAD</term>
<term>Stéatose hépatique non alcoolique</term>
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<term>Sérine</term>
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<term>Disease Models, Animal</term>
<term>Female</term>
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<term>Humans</term>
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<term>Animaux</term>
<term>Femelle</term>
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<term>Humains</term>
<term>Modèles animaux de maladie humaine</term>
<term>Modélisation spécifique au patient</term>
<term>Mâle</term>
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<front><div type="abstract" xml:lang="en">To elucidate the molecular mechanisms underlying non-alcoholic fatty liver disease (NAFLD), we recruited 86 subjects with varying degrees of hepatic steatosis (HS). We obtained experimental data on lipoprotein fluxes and used these individual measurements as personalized constraints of a hepatocyte genome-scale metabolic model to investigate metabolic differences in liver, taking into account its interactions with other tissues. Our systems level analysis predicted an altered demand for NAD(+) and glutathione (GSH) in subjects with high HS Our analysis and metabolomic measurements showed that plasma levels of glycine, serine, and associated metabolites are negatively correlated with HS, suggesting that these GSH metabolism precursors might be limiting. Quantification of the hepatic expression levels of the associated enzymes further pointed to altered de novo GSH synthesis. To assess the effect of GSH and NAD(+) repletion on the development of NAFLD, we added precursors for GSH and NAD(+) biosynthesis to the Western diet and demonstrated that supplementation prevents HS in mice. In a proof-of-concept human study, we found improved liver function and decreased HS after supplementation with serine (a precursor to glycine) and hereby propose a strategy for NAFLD treatment.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28254760</PMID>
<DateCreated><Year>2017</Year>
<Month>03</Month>
<Day>03</Day>
</DateCreated>
<DateCompleted><Year>2017</Year>
<Month>07</Month>
<Day>31</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>07</Month>
<Day>31</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1744-4292</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>13</Volume>
<Issue>3</Issue>
<PubDate><Year>2017</Year>
<Month>Mar</Month>
<Day>02</Day>
</PubDate>
</JournalIssue>
<Title>Molecular systems biology</Title>
<ISOAbbreviation>Mol. Syst. Biol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Personal model-assisted identification of NAD(+) and glutathione metabolism as intervention target in NAFLD.</ArticleTitle>
<Pagination><MedlinePgn>916</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.15252/msb.20167422</ELocationID>
<Abstract><AbstractText>To elucidate the molecular mechanisms underlying non-alcoholic fatty liver disease (NAFLD), we recruited 86 subjects with varying degrees of hepatic steatosis (HS). We obtained experimental data on lipoprotein fluxes and used these individual measurements as personalized constraints of a hepatocyte genome-scale metabolic model to investigate metabolic differences in liver, taking into account its interactions with other tissues. Our systems level analysis predicted an altered demand for NAD(+) and glutathione (GSH) in subjects with high HS Our analysis and metabolomic measurements showed that plasma levels of glycine, serine, and associated metabolites are negatively correlated with HS, suggesting that these GSH metabolism precursors might be limiting. Quantification of the hepatic expression levels of the associated enzymes further pointed to altered de novo GSH synthesis. To assess the effect of GSH and NAD(+) repletion on the development of NAFLD, we added precursors for GSH and NAD(+) biosynthesis to the Western diet and demonstrated that supplementation prevents HS in mice. In a proof-of-concept human study, we found improved liver function and decreased HS after supplementation with serine (a precursor to glycine) and hereby propose a strategy for NAFLD treatment.</AbstractText>
<CopyrightInformation>© 2017 The Authors. Published under the terms of the CC BY 4.0 license.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Mardinoglu</LastName>
<ForeName>Adil</ForeName>
<Initials>A</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-4254-6090</Identifier>
<AffiliationInfo><Affiliation>Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, Sweden adilm@scilifelab.se jan.boren@wlab.gu.se.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bjornson</LastName>
<ForeName>Elias</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Cheng</ForeName>
<Initials>C</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-3721-8586</Identifier>
<AffiliationInfo><Affiliation>Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Klevstig</LastName>
<ForeName>Martina</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Söderlund</LastName>
<ForeName>Sanni</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Research programs Unit, Diabetes and Obesity, Helsinki University Hospital, University of Helsinki, Helsinki, Finland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ståhlman</LastName>
<ForeName>Marcus</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Adiels</LastName>
<ForeName>Martin</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hakkarainen</LastName>
<ForeName>Antti</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lundbom</LastName>
<ForeName>Nina</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>Department of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kilicarslan</LastName>
<ForeName>Murat</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hallström</LastName>
<ForeName>Björn M</ForeName>
<Initials>BM</Initials>
<AffiliationInfo><Affiliation>Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lundbom</LastName>
<ForeName>Jesper</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Radiology, HUS Medical Imaging Center, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Vergès</LastName>
<ForeName>Bruno</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Department of Endocrinology-Diabetology, University Hospital and INSERM CRI 866, Dijon, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Barrett</LastName>
<ForeName>Peter Hugh R</ForeName>
<Initials>PH</Initials>
<AffiliationInfo><Affiliation>Faculty of Engineering, Computing and Mathematics, University of Western Australia, Perth, WA, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Watts</LastName>
<ForeName>Gerald F</ForeName>
<Initials>GF</Initials>
<AffiliationInfo><Affiliation>Metabolic Research Centre, Cardiovascular Medicine, Royal Perth Hospital, School of Medicine and Pharmacology, University of Western Australia, Perth, WA, Australia.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Serlie</LastName>
<ForeName>Mireille J</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo><Affiliation>Department of Endocrinology and Metabolism, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nielsen</LastName>
<ForeName>Jens</ForeName>
<Initials>J</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-9955-6003</Identifier>
<AffiliationInfo><Affiliation>Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Biology and Biological Engineering, Chalmers University of Technology, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Uhlén</LastName>
<ForeName>Mathias</ForeName>
<Initials>M</Initials>
<Identifier Source="ORCID">http://orcid.org/0000-0002-4858-8056</Identifier>
<AffiliationInfo><Affiliation>Science for Life Laboratory, KTH - Royal Institute of Technology, Stockholm, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Smith</LastName>
<ForeName>Ulf</ForeName>
<Initials>U</Initials>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Marschall</LastName>
<ForeName>Hanns-Ulrich</ForeName>
<Initials>HU</Initials>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Taskinen</LastName>
<ForeName>Marja-Riitta</ForeName>
<Initials>MR</Initials>
<AffiliationInfo><Affiliation>Research programs Unit, Diabetes and Obesity, Helsinki University Hospital, University of Helsinki, Helsinki, Finland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Boren</LastName>
<ForeName>Jan</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Molecular and Clinical Medicine, University of Gothenburg, and Sahlgrenska University Hospital, Gothenburg, Sweden adilm@scilifelab.se jan.boren@wlab.gu.se.</Affiliation>
</AffiliationInfo>
</Author>
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<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2017</Year>
<Month>03</Month>
<Day>02</Day>
</ArticleDate>
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<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Mol Syst Biol</MedlineTA>
<NlmUniqueID>101235389</NlmUniqueID>
<ISSNLinking>1744-4292</ISSNLinking>
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<NameOfSubstance UI="D005998">Glycine</NameOfSubstance>
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<CitationSubset>IM</CitationSubset>
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   |texte=   Personal model-assisted identification of NAD(+) and glutathione metabolism as intervention target in NAFLD.
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	Serveur d'exploration sur les relations entre la France et l'Australie
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Personal model-assisted identification of NAD(+) and glutathione metabolism as intervention target in NAFLD.

Personal model-assisted identification of NAD(+) and glutathione metabolism as intervention target in NAFLD.

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