Induction of TDO2 and IDO2 in Liver by High-Fat Feeding in Mice: Discrepancies with Human Obesity.
Identifieur interne : 003B36 ( PubMed/Corpus ); précédent : 003B35; suivant : 003B37Induction of TDO2 and IDO2 in Liver by High-Fat Feeding in Mice: Discrepancies with Human Obesity.
Auteurs : Odile Poulain-Godefroy ; Elodie Eury ; Audrey Leloire ; Benjamin Hennart ; Gilles J. Guillemin ; Delphine Allorge ; Philippe FroguelSource :
- 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.
DOI: 10.4137/IJTR.S11717
PubMed: 26882470
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pubmed:26882470Le document en format XML
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<front><div type="abstract" xml:lang="en">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.</div>
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<Abstract><AbstractText>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.</AbstractText>
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<CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Nature. 2008 Jan 10;451(7175):211-5</RefSource>
<PMID Version="1">18185592</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochem J. 1976 Nov 15;160(2):315-24</RefSource>
<PMID Version="1">1008859</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Ann N Y Acad Sci. 2010 Jun;1199:1-14</RefSource>
<PMID Version="1">20633104</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Endocrinology. 2004 Jun;145(6):2707-12</RefSource>
<PMID Version="1">15044372</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2010 May 25;107(21):9765-70</RefSource>
<PMID Version="1">20445103</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nature. 2011 Oct 05;478(7368):197-203</RefSource>
<PMID Version="1">21976023</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2007 May;117(5):1147-54</RefSource>
<PMID Version="1">17476344</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Proc Nutr Soc. 2011 Nov;70(4):408-17</RefSource>
<PMID Version="1">21835098</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Arterioscler Thromb Vasc Biol. 2008 Jul;28(7):1304-10</RefSource>
<PMID Version="1">18420999</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nephrol Dial Transplant. 2009 Jun;24(6):1901-8</RefSource>
<PMID Version="1">19155537</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biochem. 1983 Nov;94(5):1697-706</RefSource>
<PMID Version="1">6361014</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochem J. 1984 Feb 1;217(3):863-4</RefSource>
<PMID Version="1">6712603</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Chromatogr B Analyt Technol Biomed Life Sci. 2008 May 1;867(1):57-61</RefSource>
<PMID Version="1">18395499</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 1987 Jan 15;262(2):727-33</RefSource>
<PMID Version="1">3542992</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Nutr Res Rev. 2010 Dec;23(2):270-99</RefSource>
<PMID Version="1">20977819</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Endocr Rev. 2004 Oct;25(5):831-66</RefSource>
<PMID Version="1">15466942</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Endocrine. 2006 Feb;29(1):101-8</RefSource>
<PMID Version="1">16622297</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Gastroenterology. 2007 Aug;133(2):608-18</RefSource>
<PMID Version="1">17681180</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Endocrinol Metab. 2002 Mar;282(3):E657-63</RefSource>
<PMID Version="1">11832370</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Diabetologia. 2007 Sep;50(9):1867-79</RefSource>
<PMID Version="1">17618414</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Obes Surg. 2006 May;16(5):541-8</RefSource>
<PMID Version="1">16687019</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Cancer Immunol Immunother. 2012 Nov;61(11):2013-20</RefSource>
<PMID Version="1">22527253</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Curr Med Chem. 2011;18(15):2215-21</RefSource>
<PMID Version="1">21517758</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Sci Transl Med. 2010 May 19;2(32):32ra36</RefSource>
<PMID Version="1">20484731</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 1986 Mar 15;261(8):3648-53</RefSource>
<PMID Version="1">2419335</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Int J Biochem Cell Biol. 2009 Mar;41(3):467-71</RefSource>
<PMID Version="1">18282734</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Cell Endocrinol. 2010 Mar 25;316(2):154-64</RefSource>
<PMID Version="1">19804814</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Clin Endocrinol Metab. 2010 Dec;95(12):5419-26</RefSource>
<PMID Version="1">20843952</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Biochem J. 1985 Jul 15;229(2):499-504</RefSource>
<PMID Version="1">3899109</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Circulation. 2012 May 8;125(18):2222-31</RefSource>
<PMID Version="1">22496159</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2006 Jan;116(1):115-24</RefSource>
<PMID Version="1">16341265</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>EMBO J. 1987 Mar;6(3):625-30</RefSource>
<PMID Version="1">3582368</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Surg Obes Relat Dis. 2012 Jan-Feb;8(1):73-81</RefSource>
<PMID Version="1">21978752</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Mol Endocrinol. 2010 Mar;24(3):657-66</RefSource>
<PMID Version="1">20150186</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Steroid Biochem Mol Biol. 2010 Mar;119(1-2):56-72</RefSource>
<PMID Version="1">20045052</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Regul Integr Comp Physiol. 2012 Jul 15;303(2):R135-43</RefSource>
<PMID Version="1">22592557</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>ScientificWorldJournal. 2007 May 29;7:666-85</RefSource>
<PMID Version="1">17619751</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Am J Physiol Regul Integr Comp Physiol. 2008 Jul;295(1):R1-7</RefSource>
<PMID Version="1">18448614</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Adv Exp Med Biol. 2003;527:455-63</RefSource>
<PMID Version="1">15206763</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Biol Chem. 2011 Oct 7;286(40):34800-8</RefSource>
<PMID Version="1">21841000</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>J Immunol. 2009 Aug 15;183(4):2475-83</RefSource>
<PMID Version="1">19635913</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites"><RefSource>Am J Physiol. 1968 Jun;214(6):1410-4</RefSource>
<PMID Version="1">4384954</PMID>
</CommentsCorrections>
</CommentsCorrectionsList>
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