Induction of TDO2 and IDO2 in Liver by High-Fat Feeding in Mice: Discrepancies with Human Obesity
Identifieur interne : 002464 ( Pmc/Curation ); précédent : 002463; suivant : 002465Induction of TDO2 and IDO2 in Liver by High-Fat Feeding in Mice: Discrepancies with Human Obesity
Auteurs : Odile Poulain-Godefroy [France] ; Elodie Eury [France] ; Audrey Leloire [France] ; Benjamin Hennart [France] ; Gilles J. Guillemin [Australie] ; Delphine Allorge [France] ; Philippe Froguel [France, Royaume-Uni]Source :
- International Journal of Tryptophan Research : IJTR [ 1178-6469 ] ; 2013.
Abstract
Low-grade and chronic inflammation is elicited in white adipose tissue in human obesity. The presence of inflammatory molecules leads to an increased tryptophan catabolism through the induction of indoleamine-2,3-dioxygenase-1 (IDO1). In order to characterize the mechanisms underlying this dysregulation, we have studied 2 mouse models of obesity. Unexpectedly, we did not detect any IDO1 expression in obese or lean mice adipose tissue. In a previous study, we did not find any significant difference in the liver for IDO2 and tryptophan-2,3-dioxygenase (TDO2) gene expression between normal weight and obese patients. IDO2 and TDO2 expression was increased in the liver of high-fat fed mice, but not in ob/ob mice, and was strongly correlated with hydroxysteroid-(11-beta) dehydrogenase-1 (HSD11B1) expression, an enzyme that generates active cortisol within tissues. In conclusion, despite a dysregulation of tryptophan metabolism, obese mice display discrepancies with human obesity metabolism, rendering them inappropriate for further investigations in this animal model.
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DOI: 10.4137/IJTR.S11717
PubMed: 26882470
PubMed Central: 3729279
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Obesity</title><author><name sortKey="Poulain Godefroy, Odile" sort="Poulain Godefroy, Odile" uniqKey="Poulain Godefroy O" first="Odile" last="Poulain-Godefroy">Odile Poulain-Godefroy</name><affiliation wicri:level="1"><nlm:aff id="af1-ijtr-suppl.1-2013-029">European Genomic Institute for Diabetes (EGID), Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>European Genomic Institute for Diabetes (EGID), Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-ijtr-suppl.1-2013-029">University of Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>University of Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af3-ijtr-suppl.1-2013-029">CNRS UMR 8199, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>CNRS UMR 8199, Lille</wicri:regionArea></affiliation><affiliation 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id="af1-ijtr-suppl.1-2013-029">European Genomic Institute for Diabetes (EGID), Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>European Genomic Institute for Diabetes (EGID), Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-ijtr-suppl.1-2013-029">University of Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>University of Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af3-ijtr-suppl.1-2013-029">CNRS UMR 8199, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>CNRS UMR 8199, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-ijtr-suppl.1-2013-029">CHRU Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>CHRU Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af5-ijtr-suppl.1-2013-029">IPL, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>IPL, Lille</wicri:regionArea></affiliation></author><author><name sortKey="Hennart, Benjamin" sort="Hennart, Benjamin" uniqKey="Hennart B" first="Benjamin" last="Hennart">Benjamin Hennart</name><affiliation wicri:level="1"><nlm:aff id="af2-ijtr-suppl.1-2013-029">University of Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>University of Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-ijtr-suppl.1-2013-029">CHRU Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>CHRU Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af6-ijtr-suppl.1-2013-029">EA4483, Faculty of Medicine, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>EA4483, Faculty of Medicine, Lille</wicri:regionArea></affiliation></author><author><name sortKey="Guillemin, Gilles J" sort="Guillemin, Gilles J" uniqKey="Guillemin G" first="Gilles J." last="Guillemin">Gilles J. Guillemin</name><affiliation wicri:level="1"><nlm:aff id="af7-ijtr-suppl.1-2013-029">MND and Neurodegenerative Diseases Research Group, Australian School of Advanced Medicine, Macquarie University, Australia.</nlm:aff><country xml:lang="fr" wicri:curation="lc">Australie</country><wicri:regionArea>MND and Neurodegenerative Diseases Research Group, Australian School of Advanced Medicine, Macquarie University</wicri:regionArea></affiliation></author><author><name sortKey="Allorge, Delphine" sort="Allorge, Delphine" uniqKey="Allorge D" first="Delphine" last="Allorge">Delphine Allorge</name><affiliation wicri:level="1"><nlm:aff id="af2-ijtr-suppl.1-2013-029">University of Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>University of Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-ijtr-suppl.1-2013-029">CHRU Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>CHRU Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af6-ijtr-suppl.1-2013-029">EA4483, Faculty of Medicine, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>EA4483, Faculty of Medicine, Lille</wicri:regionArea></affiliation></author><author><name sortKey="Froguel, Philippe" sort="Froguel, Philippe" uniqKey="Froguel P" first="Philippe" last="Froguel">Philippe Froguel</name><affiliation wicri:level="1"><nlm:aff id="af1-ijtr-suppl.1-2013-029">European Genomic Institute for Diabetes (EGID), Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>European Genomic Institute for Diabetes (EGID), Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-ijtr-suppl.1-2013-029">University of Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>University of Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af3-ijtr-suppl.1-2013-029">CNRS UMR 8199, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>CNRS UMR 8199, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af4-ijtr-suppl.1-2013-029">CHRU Lille, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>CHRU Lille, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af5-ijtr-suppl.1-2013-029">IPL, Lille, France.</nlm:aff><country xml:lang="fr" wicri:curation="lc">France</country><wicri:regionArea>IPL, Lille</wicri:regionArea></affiliation><affiliation wicri:level="1"><nlm:aff id="af8-ijtr-suppl.1-2013-029">Department of Genomics of Common Disease, School of Public Health, Imperial College London, United Kingdom.</nlm:aff><country xml:lang="fr" wicri:curation="lc">Royaume-Uni</country><wicri:regionArea>Department of Genomics of Common Disease, School of Public Health, Imperial College London</wicri:regionArea></affiliation></author></analytic><series><title level="j">International Journal of Tryptophan Research : IJTR</title><idno type="eISSN">1178-6469</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Low-grade and chronic inflammation is elicited in white adipose tissue in human obesity. The presence of inflammatory molecules leads to an increased tryptophan catabolism through the induction of indoleamine-2,3-dioxygenase-1 (IDO1). In order to characterize the mechanisms underlying this dysregulation, we have studied 2 mouse models of obesity. Unexpectedly, we did not detect any IDO1 expression in obese or lean mice adipose tissue. In a previous study, we did not find any significant difference in the liver for IDO2 and tryptophan-2,3-dioxygenase (TDO2) gene expression between normal weight and obese patients. IDO2 and TDO2 expression was increased in the liver of high-fat fed mice, but not in ob/ob mice, and was strongly correlated with hydroxysteroid-(11-beta) dehydrogenase-1 (HSD11B1) expression, an enzyme that generates active cortisol within tissues. In conclusion, despite a dysregulation of tryptophan metabolism, obese mice display discrepancies with human obesity metabolism, rendering them inappropriate for further investigations in this animal model.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Harford, Ka" uniqKey="Harford K">KA Harford</name></author><author><name sortKey="Reynolds, Cm" uniqKey="Reynolds C">CM Reynolds</name></author><author><name sortKey="Mcgillicuddy, Fc" uniqKey="Mcgillicuddy F">FC McGillicuddy</name></author><author><name sortKey="Roche, Hm" uniqKey="Roche H">HM Roche</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Liu, J" uniqKey="Liu J">J Liu</name></author><author><name sortKey="Fox, Cs" uniqKey="Fox C">CS Fox</name></author><author><name sortKey="Hickson, Da" uniqKey="Hickson D">DA Hickson</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Wolowczuk, I" uniqKey="Wolowczuk I">I 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Tryptophan Res</journal-id><journal-id journal-id-type="iso-abbrev">Int J Tryptophan Res</journal-id><journal-title-group><journal-title>International Journal of Tryptophan Research : IJTR</journal-title></journal-title-group><issn pub-type="epub">1178-6469</issn><publisher><publisher-name>Libertas Academica</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">26882470</article-id><article-id pub-id-type="pmc">3729279</article-id><article-id pub-id-type="doi">10.4137/IJTR.S11717</article-id><article-id pub-id-type="publisher-id">ijtr-suppl_1-2013-029</article-id><article-categories><subj-group subj-group-type="heading"><subject>Meeting Report</subject></subj-group></article-categories><title-group><article-title>Induction of TDO2 and IDO2 in Liver by High-Fat Feeding in Mice: Discrepancies with Human Obesity</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Poulain-Godefroy</surname><given-names>Odile</given-names></name><xref ref-type="aff" rid="af1-ijtr-suppl.1-2013-029">1</xref><xref ref-type="aff" rid="af2-ijtr-suppl.1-2013-029">2</xref><xref ref-type="aff" rid="af3-ijtr-suppl.1-2013-029">3</xref><xref ref-type="aff" rid="af4-ijtr-suppl.1-2013-029">4</xref><xref ref-type="aff" rid="af5-ijtr-suppl.1-2013-029">5</xref><xref ref-type="corresp" rid="c1-ijtr-suppl.1-2013-029"></xref></contrib><contrib contrib-type="author"><name><surname>Eury</surname><given-names>Elodie</given-names></name><xref ref-type="aff" rid="af1-ijtr-suppl.1-2013-029">1</xref><xref ref-type="aff" rid="af2-ijtr-suppl.1-2013-029">2</xref><xref ref-type="aff" rid="af3-ijtr-suppl.1-2013-029">3</xref><xref ref-type="aff" rid="af4-ijtr-suppl.1-2013-029">4</xref><xref ref-type="aff" rid="af5-ijtr-suppl.1-2013-029">5</xref></contrib><contrib contrib-type="author"><name><surname>Leloire</surname><given-names>Audrey</given-names></name><xref ref-type="aff" rid="af1-ijtr-suppl.1-2013-029">1</xref><xref ref-type="aff" rid="af2-ijtr-suppl.1-2013-029">2</xref><xref ref-type="aff" rid="af3-ijtr-suppl.1-2013-029">3</xref><xref ref-type="aff" rid="af4-ijtr-suppl.1-2013-029">4</xref><xref ref-type="aff" rid="af5-ijtr-suppl.1-2013-029">5</xref></contrib><contrib contrib-type="author"><name><surname>Hennart</surname><given-names>Benjamin</given-names></name><xref ref-type="aff" rid="af2-ijtr-suppl.1-2013-029">2</xref><xref ref-type="aff" rid="af4-ijtr-suppl.1-2013-029">4</xref><xref ref-type="aff" rid="af6-ijtr-suppl.1-2013-029">6</xref></contrib><contrib contrib-type="author"><name><surname>Guillemin</surname><given-names>Gilles J.</given-names></name><xref ref-type="aff" rid="af7-ijtr-suppl.1-2013-029">7</xref></contrib><contrib contrib-type="author"><name><surname>Allorge</surname><given-names>Delphine</given-names></name><xref ref-type="aff" rid="af2-ijtr-suppl.1-2013-029">2</xref><xref ref-type="aff" rid="af4-ijtr-suppl.1-2013-029">4</xref><xref ref-type="aff" rid="af6-ijtr-suppl.1-2013-029">6</xref></contrib><contrib contrib-type="author"><name><surname>Froguel</surname><given-names>Philippe</given-names></name><xref ref-type="aff" rid="af1-ijtr-suppl.1-2013-029">1</xref><xref ref-type="aff" rid="af2-ijtr-suppl.1-2013-029">2</xref><xref ref-type="aff" rid="af3-ijtr-suppl.1-2013-029">3</xref><xref ref-type="aff" rid="af4-ijtr-suppl.1-2013-029">4</xref><xref ref-type="aff" rid="af5-ijtr-suppl.1-2013-029">5</xref><xref ref-type="aff" rid="af8-ijtr-suppl.1-2013-029">8</xref></contrib></contrib-group><aff id="af1-ijtr-suppl.1-2013-029"><label>1</label>European Genomic Institute for Diabetes (EGID), Lille, France.</aff><aff id="af2-ijtr-suppl.1-2013-029"><label>2</label>University of Lille, Lille, France.</aff><aff id="af3-ijtr-suppl.1-2013-029"><label>3</label>CNRS UMR 8199, Lille, France.</aff><aff id="af4-ijtr-suppl.1-2013-029"><label>4</label>CHRU Lille, Lille, France.</aff><aff id="af5-ijtr-suppl.1-2013-029"><label>5</label>IPL, Lille, France.</aff><aff id="af6-ijtr-suppl.1-2013-029"><label>6</label>EA4483, Faculty of Medicine, Lille, France.</aff><aff id="af7-ijtr-suppl.1-2013-029"><label>7</label>MND and Neurodegenerative Diseases Research Group, Australian School of Advanced Medicine, Macquarie University, Australia.</aff><aff id="af8-ijtr-suppl.1-2013-029"><label>8</label>Department of Genomics of Common Disease, School of Public Health, Imperial College London, United Kingdom.</aff><author-notes><corresp id="c1-ijtr-suppl.1-2013-029">Corresponding author email: <email>odile.poulain@good.ibl.fr</email></corresp></author-notes><pub-date pub-type="collection"><year>2013</year></pub-date><pub-date pub-type="epub"><day>21</day><month>7</month><year>2013</year></pub-date><volume>6</volume><issue>Suppl 1</issue><fpage>29</fpage><lpage>37</lpage><permissions><copyright-statement>© 2013 the author(s), publisher and licensee Libertas Academica Ltd.</copyright-statement><copyright-year>2013</copyright-year><license license-type="open-access"><license-p>This is an open access article published under the Creative Commons CC-BY-NC 3.0 license.</license-p></license></permissions><abstract><p>Low-grade and chronic inflammation is elicited in white adipose tissue in human obesity. The presence of inflammatory molecules leads to an increased tryptophan catabolism through the induction of indoleamine-2,3-dioxygenase-1 (IDO1). In order to characterize the mechanisms underlying this dysregulation, we have studied 2 mouse models of obesity. Unexpectedly, we did not detect any IDO1 expression in obese or lean mice adipose tissue. In a previous study, we did not find any significant difference in the liver for IDO2 and tryptophan-2,3-dioxygenase (TDO2) gene expression between normal weight and obese patients. IDO2 and TDO2 expression was increased in the liver of high-fat fed mice, but not in ob/ob mice, and was strongly correlated with hydroxysteroid-(11-beta) dehydrogenase-1 (HSD11B1) expression, an enzyme that generates active cortisol within tissues. In conclusion, despite a dysregulation of tryptophan metabolism, obese mice display discrepancies with human obesity metabolism, rendering them inappropriate for further investigations in this animal model.</p></abstract><kwd-group><kwd>tryptophan 2</kwd><kwd>3-dioxygenase</kwd><kwd>indoleamine 2</kwd><kwd>3-dioxygenase 2</kwd><kwd>obesity</kwd><kwd>high fat diet</kwd></kwd-group></article-meta></front><floats-group><fig id="f1-ijtr-suppl.1-2013-029" position="float"><label>Figure 1</label><caption><p>Six-week-old C57Bl6J male mice were fed either a standard diet (○) or a high-fat diet (●); n = 40/group. N = 8 in each group were sacrificed every 3 weeks. (<bold>A</bold>) Body weight was expressed as a percentage of initial mass. (<bold>B</bold>) Left epidydimal adipose tissue mass was expressed as a percentage of total body weight (<bold>C</bold>) Intraperitoneal glucose tolerance test with 1 g glucose/kg body mass after 6 hr of fasting performed on animals after 16 weeks of diet.</p><p><bold>Notes: ***</bold><italic>P</italic> < 0.001; **<italic>P</italic> < 0.005; *<italic>P</italic> < 0.05.</p></caption><graphic xlink:href="ijtr-suppl.1-2013-029f1"></graphic></fig><fig id="f2-ijtr-suppl.1-2013-029" position="float"><label>Figure 2</label><caption><p>(<bold>A</bold>) Expression of CCL2 in epidymal adipose tissue of mice: C57Bl/6J fed either a standard diet (white) or a high fat diet (black) n = 40/group. N = 8 in each group were sacrificed every 3 weeks (week 4 to week 16)—or 6 hours after an intraperitoneal administration of LPS (vehicle: white; LPS: black; n = 8)—or of ob/ob mice (control littermate: white; OB/OB: black; n = 5). (<bold>B</bold>) Expression of IDO1 in epidydimal adipose tissue of mice: C57Bl/6J fed either a standard diet (control) or a high fat diet (HFD) for 16 weeks (n = 8)—or 6 hours after an intraperitoneal administration of LPS (LPS; n = 8)—or of ob/ob mice (OB/OB; n = 5). (<bold>C</bold>) Kynurenine/tryptophan ratio in pooled sera of C57Bl/6J fed either a standard diet (white) or a high fat diet (black) for 16 weeks; n = 40/group. N = 8 in each group were sacrificed every 3 weeks and corresponding sera were pooled—or 6 hours after an intraperitoneal administration of LPS (vehicle: white; LPS: black; n = 8).</p><p><bold>Notes:</bold> ***<italic>P</italic> < 0.001; **<italic>P</italic> < 0.005; *<italic>P</italic> < 0.05.</p></caption><graphic xlink:href="ijtr-suppl.1-2013-029f2"></graphic></fig><fig id="f3-ijtr-suppl.1-2013-029" position="float"><label>Figure 3</label><caption><p>Expression of IDO2 (<bold>A</bold>) and of TDO2 (<bold>B</bold>) in hepatic tissue of mice: C57Bl/6J fed either a standard diet (white) or a high fat diet (black) n = 40/group. N = 8 in each group were sacrificed every 3 weeks (week 4 to week 16)—or 6 hours after an intraperitoneal administration of LPS (vehicle: white; LPS: black; n = 8)—or of ob/ob mice (control littermate: white; OB/OB: black; n = 5). (<bold>C</bold>) Correlation between TDO2 and IDO2 expression in hepatic tissue of C57Bl/6J mice after 16 weeks of standard diet (○) or high-fat diet (●); Pearson analysis.</p><p><bold>Notes:</bold> ***<italic>P</italic> < 0.001; **<italic>P</italic> < 0.005; *<italic>P</italic> < 0.05.</p></caption><graphic xlink:href="ijtr-suppl.1-2013-029f3"></graphic></fig><fig id="f4-ijtr-suppl.1-2013-029" position="float"><label>Figure 4</label><caption><p>Correlation between IDO2 or TDO2 and HSD11B1 expression in hepatic tissue (Pearson analysis). (<bold>A</bold>) C57Bl/6J fed during 16 weeks either a standard diet (○) or a high fat diet (●) IDO2: r<sup>2</sup> = 0.806 (<italic>P</italic> = 0.016) for high fat diet and r<sup>2</sup> = 0,847 (<italic>P</italic> = 0.008) for control TDO2: r<sup>2</sup> = 0.825 (<italic>P</italic> = 0.012) for high fat diet and r<sup>2</sup> = 0.829 (<italic>P</italic> = 0.011) for control. (<bold>B</bold>) ob/ob (●) or littermate control (○) IDO2: r<sup>2</sup> = 0.742 (<italic>P</italic> = 0.0014) TDO2: r<sup>2</sup> = 0.816 (<italic>P</italic> = 0.0003). (<bold>C</bold>) 6 hours after an intraperitoneal administration of LPS (●) or vehicle (○); IDO2 expression r<sup>2</sup> = 0.943 (<italic>P</italic> < 0.0001).</p></caption><graphic xlink:href="ijtr-suppl.1-2013-029f4"></graphic></fig></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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