Personal model‐assisted identification of NAD+ and glutathione metabolism as intervention target in NAFLD

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...

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Published inMolecular systems biology Vol. 13; no. 3; pp. 916 - n/a
Main Authors Mardinoglu, Adil, Bjornson, Elias, Zhang, Cheng, Klevstig, Martina, Söderlund, Sanni, Ståhlman, Marcus, Adiels, Martin, Hakkarainen, Antti, Lundbom, Nina, Kilicarslan, Murat, Hallström, Björn M, Lundbom, Jesper, Vergès, Bruno, Barrett, Peter Hugh R, Watts, Gerald F, Serlie, Mireille J, Nielsen, Jens, Uhlén, Mathias, Smith, Ulf, Marschall, Hanns‐Ulrich, Taskinen, Marja‐Riitta, Boren, Jan
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.03.2017
EMBO Press
John Wiley and Sons Inc
Springer Nature
Subjects
1976
1991
adipose-tissue
amino-acid-metabolism
Animals
Apolipoproteins
Biochemistry & Molecular Biology
Biosynthesis
Body mass index
british journal of nutrition
Cholesterol
Demand analysis
Dietary supplements
Disease Models, Animal
drug targets
EMBO17
EMBO21
EMBO42
Fasting
Fatty liver
fatty liver-disease
Female
Fluxes
Gene expression
Gene Expression Regulation, Enzymologic
Genome
genome-scale
Genomes
Glutathione
Glutathione - metabolism
Glycine
Glycine - blood
hepatocellular-carcinoma
Humans
Insulin resistance
journal of clinical investigation
Laboratory animals
Life Sciences
Lipids
Lipoproteins - metabolism
Liver
Liver - enzymology
Liver - metabolism
Liver diseases
Male
Metabolism
Metabolites
Metabolomics
Metabolomics - methods
Mice
Middle Aged
Molecular Biology
Molecular modelling
Molekylärbiologi
muscle
NAD
NAD - metabolism
NAFLD
Non-alcoholic Fatty Liver Disease - diet therapy
Non-alcoholic Fatty Liver Disease - genetics
Non-alcoholic Fatty Liver Disease - metabolism
obesity
p105
p444
Patient-Specific Modeling
personalized genome-scale metabolic modeling
Plasma levels
Precursors
Serine
Serine - administration & dosage
Serine - blood
Serine - therapeutic use
Steatosis
tissue blood-flow
Triglycerides
urenberg p
v57
v65
zefsky t
United States > US
serine
NAFLD
personalized genome‐scale metabolic modeling
glutathione
Online AccessGet full text
ISSN1744-4292
1744-4292
DOI10.15252/msb.20167422

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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. Synopsis Personalized modeling and metabolic measurements identified altered GSH and NAD + metabolism as a prevailing feature in NAFLD. These findings suggested a potential treatment strategy for NAFLD patients based on increased oxidation of fat and increased synthesis of GSH. We developed personalized genome‐scale metabolic models for NAFLD patients. We found that altered GSH and NAD + metabolism is a prevailing feature in NAFLD. Plasma and liver levels of glycine and serine were lower in NAFLD patients. Supplementation of precursors for glutathione and NAD + decreased HS in mice. Serine supplementation decreased liver fat and improved markers of liver function in humans. Graphical Abstract Personalized modeling and metabolic measurements identified altered GSH and NAD + metabolism as a prevailing feature in NAFLD. These findings suggested a potential treatment strategy for NAFLD patients based on increased oxidation of fat and increased synthesis of GSH.
AbstractList 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. Synopsis Personalized modeling and metabolic measurements identified altered GSH and NAD + metabolism as a prevailing feature in NAFLD. These findings suggested a potential treatment strategy for NAFLD patients based on increased oxidation of fat and increased synthesis of GSH. We developed personalized genome‐scale metabolic models for NAFLD patients. We found that altered GSH and NAD + metabolism is a prevailing feature in NAFLD. Plasma and liver levels of glycine and serine were lower in NAFLD patients. Supplementation of precursors for glutathione and NAD + decreased HS in mice. Serine supplementation decreased liver fat and improved markers of liver function in humans. Graphical Abstract Personalized modeling and metabolic measurements identified altered GSH and NAD + metabolism as a prevailing feature in NAFLD. These findings suggested a potential treatment strategy for NAFLD patients based on increased oxidation of fat and increased synthesis of GSH.
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.
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.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.
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.
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.
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. image Personalized modeling and metabolic measurements identified altered GSH and NAD + metabolism as a prevailing feature in NAFLD . These findings suggested a potential treatment strategy for NAFLD patients based on increased oxidation of fat and increased synthesis of GSH . We developed personalized genome‐scale metabolic models for NAFLD patients. We found that altered GSH and NAD + metabolism is a prevailing feature in NAFLD . Plasma and liver levels of glycine and serine were lower in NAFLD patients. Supplementation of precursors for glutathione and NAD + decreased HS in mice. Serine supplementation decreased liver fat and improved markers of liver function in humans.
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 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.
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. Synopsis Personalized modeling and metabolic measurements identified altered GSH and NAD+ metabolism as a prevailing feature in NAFLD. These findings suggested a potential treatment strategy for NAFLD patients based on increased oxidation of fat and increased synthesis of GSH. We developed personalized genome‐scale metabolic models for NAFLD patients. We found that altered GSH and NAD+ metabolism is a prevailing feature in NAFLD. Plasma and liver levels of glycine and serine were lower in NAFLD patients. Supplementation of precursors for glutathione and NAD+ decreased HS in mice. Serine supplementation decreased liver fat and improved markers of liver function in humans. Personalized modeling and metabolic measurements identified altered GSH and NAD+ metabolism as a prevailing feature in NAFLD. These findings suggested a potential treatment strategy for NAFLD patients based on increased oxidation of fat and increased synthesis of GSH.
Author Mardinoglu, Adil
Serlie, Mireille J
Marschall, Hanns‐Ulrich
Zhang, Cheng
Uhlén, Mathias
Lundbom, Nina
Adiels, Martin
Kilicarslan, Murat
Vergès, Bruno
Smith, Ulf
Söderlund, Sanni
Nielsen, Jens
Boren, Jan
Watts, Gerald F
Hakkarainen, Antti
Klevstig, Martina
Ståhlman, Marcus
Lundbom, Jesper
Hallström, Björn M
Taskinen, Marja‐Riitta
Bjornson, Elias
Barrett, Peter Hugh R
AuthorAffiliation 8 Faculty of Engineering Computing and Mathematics University of Western Australia Perth WA Australia
2 Department of Biology and Biological Engineering Chalmers University of Technology Gothenburg Sweden
4 Research programs Unit Diabetes and Obesity Helsinki University Hospital University of Helsinki Helsinki Finland
7 Department of Endocrinology–Diabetology University Hospital and INSERM CRI 866 Dijon France
1 Science for Life Laboratory KTH – Royal Institute of Technology Stockholm Sweden
3 Department of Molecular and Clinical Medicine University of Gothenburg, and Sahlgrenska University Hospital Gothenburg Sweden
9 Metabolic Research Centre Cardiovascular Medicine Royal Perth Hospital School of Medicine and Pharmacology University of Western Australia Perth WA Australia
5 Department of Radiology HUS Medical Imaging Center Helsinki University Central Hospital University of Helsinki Helsinki Finland
6 Department of Endocrinology and Metabolism Academic Medical Center University of Amsterdam
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– name: 4 Research programs Unit Diabetes and Obesity Helsinki University Hospital University of Helsinki Helsinki Finland
– name: 2 Department of Biology and Biological Engineering Chalmers University of Technology Gothenburg Sweden
– name: 7 Department of Endocrinology–Diabetology University Hospital and INSERM CRI 866 Dijon France
– name: 8 Faculty of Engineering Computing and Mathematics University of Western Australia Perth WA Australia
– name: 6 Department of Endocrinology and Metabolism Academic Medical Center University of Amsterdam Amsterdam The Netherlands
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/28254760$$D View this record in MEDLINE/PubMed
https://ube.hal.science/hal-01561136$$DView record in HAL
https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-204067$$DView record from Swedish Publication Index
https://gup.ub.gu.se/publication/251601$$DView record from Swedish Publication Index
https://research.chalmers.se/publication/248745$$DView record from Swedish Publication Index
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Issue 3
Keywords serine
NAFLD
personalized genome‐scale metabolic modeling
glutathione
Language English
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2017 The Authors. Published under the terms of the CC BY 4.0 license.
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SSID ssj0038182
Score 2.5518281
Snippet To elucidate the molecular mechanisms underlying non‐alcoholic fatty liver disease (NAFLD), we recruited 86 subjects with varying degrees of hepatic steatosis...
To elucidate the molecular mechanisms underlying non‐alcoholic fatty liver disease ( NAFLD ), we recruited 86 subjects with varying degrees of hepatic...
To elucidate the molecular mechanisms underlying non-alcoholic fatty liver disease (NAFLD), we recruited 86 subjects with varying degrees of hepatic steatosis...
Abstract To elucidate the molecular mechanisms underlying non‐alcoholic fatty liver disease (NAFLD), we recruited 86 subjects with varying degrees of hepatic...
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pubmedcentral
hal
proquest
pubmed
crossref
wiley
springer
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 916
SubjectTerms 1976
1991
adipose-tissue
amino-acid-metabolism
Animals
Apolipoproteins
Biochemistry & Molecular Biology
Biosynthesis
Body mass index
british journal of nutrition
Cholesterol
Demand analysis
Dietary supplements
Disease Models, Animal
drug targets
EMBO17
EMBO21
EMBO42
Fasting
Fatty liver
fatty liver-disease
Female
Fluxes
Gene expression
Gene Expression Regulation, Enzymologic
Genome
genome-scale
Genomes
Glutathione
Glutathione - metabolism
Glycine
Glycine - blood
hepatocellular-carcinoma
Humans
Insulin resistance
journal of clinical investigation
Laboratory animals
Life Sciences
Lipids
Lipoproteins - metabolism
Liver
Liver - enzymology
Liver - metabolism
Liver diseases
Male
Metabolism
Metabolites
Metabolomics
Metabolomics - methods
Mice
Middle Aged
Molecular Biology
Molecular modelling
Molekylärbiologi
muscle
NAD
NAD - metabolism
NAFLD
Non-alcoholic Fatty Liver Disease - diet therapy
Non-alcoholic Fatty Liver Disease - genetics
Non-alcoholic Fatty Liver Disease - metabolism
obesity
p105
p444
Patient-Specific Modeling
personalized genome-scale metabolic modeling
Plasma levels
Precursors
Serine
Serine - administration & dosage
Serine - blood
Serine - therapeutic use
Steatosis
tissue blood-flow
Triglycerides
urenberg p
v57
v65
zefsky t
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Title Personal model‐assisted identification of NAD+ and glutathione metabolism as intervention target in NAFLD
URI https://link.springer.com/article/10.15252/msb.20167422
https://onlinelibrary.wiley.com/doi/abs/10.15252%2Fmsb.20167422
https://www.ncbi.nlm.nih.gov/pubmed/28254760
https://www.proquest.com/docview/2290609140
https://www.proquest.com/docview/1874445323
https://ube.hal.science/hal-01561136
https://pubmed.ncbi.nlm.nih.gov/PMC5371732
https://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-204067
https://gup.ub.gu.se/publication/251601
https://research.chalmers.se/publication/248745
https://doaj.org/article/e43610ba34b24032ab9bcfbc35617cd8
Volume 13
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