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.
Url:
DOI: 10.4137/IJTR.S11717
PubMed: 26882470
PubMed Central: 3729279
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<series><title level="j">International Journal of Tryptophan Research : IJTR</title>
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<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>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<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>
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