Gut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice
Identifieur interne : 000803 ( Main/Exploration ); précédent : 000802; suivant : 000804Gut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice
Auteurs : Robert Caesar [Suède] ; Christopher S. Reigstad [Suède] ; Helene Kling B Ckhed [Suède] ; Christoph Reinhardt [Suède] ; Maria Ketonen [Suède] ; Gunnel Östergren Lundén [Suède] ; Patrice D. Cani [Belgique] ; Fredrik B Ckhed [Suède]Source :
- Gut [ 0017-5749 ] ; 2012-12.
Abstract
Background Obesity is associated with accumulation of macrophages in white adipose tissue (WAT), which contribute to the development of insulin resistance. Germ-free (GF) mice have reduced adiposity and are protected against diet-induced obesity, Objective To investigate whether the gut microbiota and, specifically, gut-derived lipopolysaccharide (LPS) promote WAT inflammation and contribute to impaired glucose metabolism. Method Macrophage composition and expression of proinflammatory and anti-inflammatory markers were compared in WAT of GF, conventionally raised and Escherichia coli-monocolonised mice. Additionally, glucose and insulin tolerance in these mice was determined. Results The presence of a gut microbiota resulted in impaired glucose metabolism and increased macrophage accumulation and polarisation towards the proinflammatory M1 phenotype in WAT. Monocolonisation of GF mice for 4 weeks with E.coli W3110 or the isogenic strain MLK1067 (which expresses LPS with reduced immunogenicity) resulted in impaired glucose and insulin tolerance and promoted M1 polarisation of CD11b cells in WAT. However, colonisation with E.coli W3110 but not MLK1067 promoted macrophage accumulation and upregulation of proinflammatory and anti-inflammatory gene expression as well as JNK phosphorylation. Conclusion Gut microbiota induced LPS-dependent macrophage accumulation in WAT, whereas impairment of systemic glucose metabolism was not dependent on LPS. These results indicate that macrophage accumulation in WAT does not always correlate with impaired glucose metabolism.
Url:
DOI: 10.1136/gutjnl-2011-301689
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 001093
- to stream Istex, to step Curation: 001069
- to stream Istex, to step Checkpoint: 000416
- to stream Main, to step Merge: 000804
- to stream Main, to step Curation: 000803
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>Gut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice</title><author><name sortKey="Caesar, Robert" sort="Caesar, Robert" uniqKey="Caesar R" first="Robert" last="Caesar">Robert Caesar</name></author><author><name sortKey="Reigstad, Christopher S" sort="Reigstad, Christopher S" uniqKey="Reigstad C" first="Christopher S" last="Reigstad">Christopher S. Reigstad</name></author><author><name sortKey="B Ckhed, Helene Kling" sort="B Ckhed, Helene Kling" uniqKey="B Ckhed H" first="Helene Kling" last="B Ckhed">Helene Kling B Ckhed</name></author><author><name sortKey="Reinhardt, Christoph" sort="Reinhardt, Christoph" uniqKey="Reinhardt C" first="Christoph" last="Reinhardt">Christoph Reinhardt</name></author><author><name sortKey="Ketonen, Maria" sort="Ketonen, Maria" uniqKey="Ketonen M" first="Maria" last="Ketonen">Maria Ketonen</name></author><author><name sortKey="Ostergren Lunden, Gunnel" sort="Ostergren Lunden, Gunnel" uniqKey="Ostergren Lunden G" first="Gunnel" last="Östergren Lundén">Gunnel Östergren Lundén</name></author><author><name sortKey="Cani, Patrice D" sort="Cani, Patrice D" uniqKey="Cani P" first="Patrice D" last="Cani">Patrice D. Cani</name></author><author><name sortKey="B Ckhed, Fredrik" sort="B Ckhed, Fredrik" uniqKey="B Ckhed F" first="Fredrik" last="B Ckhed">Fredrik B Ckhed</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:81B5D4FCEF105E2B57956CC223B59452F03032A2</idno><date when="2012" year="2012">2012</date><idno type="doi">10.1136/gutjnl-2011-301689</idno><idno type="url">https://api.istex.fr/document/81B5D4FCEF105E2B57956CC223B59452F03032A2/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001093</idno><idno type="wicri:Area/Istex/Curation">001069</idno><idno type="wicri:Area/Istex/Checkpoint">000416</idno><idno type="wicri:doubleKey">0017-5749:2012:Caesar R:gut:derived:lipopolysaccharide</idno><idno type="wicri:Area/Main/Merge">000804</idno><idno type="wicri:Area/Main/Curation">000803</idno><idno type="wicri:Area/Main/Exploration">000803</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Gut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice</title><author><name sortKey="Caesar, Robert" sort="Caesar, Robert" uniqKey="Caesar R" first="Robert" last="Caesar">Robert Caesar</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation></author><author><name sortKey="Reigstad, Christopher S" sort="Reigstad, Christopher S" uniqKey="Reigstad C" first="Christopher S" last="Reigstad">Christopher S. Reigstad</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation></author><author><name sortKey="B Ckhed, Helene Kling" sort="B Ckhed, Helene Kling" uniqKey="B Ckhed H" first="Helene Kling" last="B Ckhed">Helene Kling B Ckhed</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Suède</country></affiliation></author><author><name sortKey="Reinhardt, Christoph" sort="Reinhardt, Christoph" uniqKey="Reinhardt C" first="Christoph" last="Reinhardt">Christoph Reinhardt</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation></author><author><name sortKey="Ketonen, Maria" sort="Ketonen, Maria" uniqKey="Ketonen M" first="Maria" last="Ketonen">Maria Ketonen</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation></author><author><name sortKey="Ostergren Lunden, Gunnel" sort="Ostergren Lunden, Gunnel" uniqKey="Ostergren Lunden G" first="Gunnel" last="Östergren Lundén">Gunnel Östergren Lundén</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation></author><author><name sortKey="Cani, Patrice D" sort="Cani, Patrice D" uniqKey="Cani P" first="Patrice D" last="Cani">Patrice D. Cani</name><affiliation wicri:level="4"><country xml:lang="fr">Belgique</country><wicri:regionArea>Université catholique de Louvain, Louvain Drug Research Institute, Metabolism and Nutrition Research Group, Brussels</wicri:regionArea><placeName><settlement type="city">Bruxelles</settlement><region nuts="2">Région de Bruxelles-Capitale</region></placeName><orgName type="university">Université catholique de Louvain</orgName></affiliation></author><author><name sortKey="B Ckhed, Fredrik" sort="B Ckhed, Fredrik" uniqKey="B Ckhed F" first="Fredrik" last="B Ckhed">Fredrik B Ckhed</name><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Sahlgrenska Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Molecular and Clinical Medicine, University of Gothenburg, Gothenburg</wicri:regionArea><wicri:noRegion>Gothenburg</wicri:noRegion></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Suède</country></affiliation></author></analytic><monogr></monogr><series><title level="j">Gut</title><title level="j" type="abbrev">Gut</title><idno type="ISSN">0017-5749</idno><idno type="eISSN">1468-3288</idno><imprint><publisher>BMJ Publishing Group Ltd and British Society of Gastroenterology</publisher><date type="published" when="2012-12">2012-12</date><biblScope unit="volume">61</biblScope><biblScope unit="issue">12</biblScope><biblScope unit="page" from="1701">1701</biblScope></imprint><idno type="ISSN">0017-5749</idno></series><idno type="istex">81B5D4FCEF105E2B57956CC223B59452F03032A2</idno><idno type="DOI">10.1136/gutjnl-2011-301689</idno><idno type="href">gutjnl-61-1701.pdf</idno><idno type="ArticleID">gutjnl-2011-301689</idno><idno type="PMID">22535377</idno><idno type="local">gutjnl;61/12/1701</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0017-5749</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Background Obesity is associated with accumulation of macrophages in white adipose tissue (WAT), which contribute to the development of insulin resistance. Germ-free (GF) mice have reduced adiposity and are protected against diet-induced obesity, Objective To investigate whether the gut microbiota and, specifically, gut-derived lipopolysaccharide (LPS) promote WAT inflammation and contribute to impaired glucose metabolism. Method Macrophage composition and expression of proinflammatory and anti-inflammatory markers were compared in WAT of GF, conventionally raised and Escherichia coli-monocolonised mice. Additionally, glucose and insulin tolerance in these mice was determined. Results The presence of a gut microbiota resulted in impaired glucose metabolism and increased macrophage accumulation and polarisation towards the proinflammatory M1 phenotype in WAT. Monocolonisation of GF mice for 4 weeks with E.coli W3110 or the isogenic strain MLK1067 (which expresses LPS with reduced immunogenicity) resulted in impaired glucose and insulin tolerance and promoted M1 polarisation of CD11b cells in WAT. However, colonisation with E.coli W3110 but not MLK1067 promoted macrophage accumulation and upregulation of proinflammatory and anti-inflammatory gene expression as well as JNK phosphorylation. Conclusion Gut microbiota induced LPS-dependent macrophage accumulation in WAT, whereas impairment of systemic glucose metabolism was not dependent on LPS. These results indicate that macrophage accumulation in WAT does not always correlate with impaired glucose metabolism.</div></front></TEI><affiliations><list><country><li>Belgique</li><li>Suède</li></country><region><li>Région de Bruxelles-Capitale</li></region><settlement><li>Bruxelles</li></settlement><orgName><li>Université catholique de Louvain</li></orgName></list><tree><country name="Suède"><noRegion><name sortKey="Caesar, Robert" sort="Caesar, Robert" uniqKey="Caesar R" first="Robert" last="Caesar">Robert Caesar</name></noRegion><name sortKey="B Ckhed, Fredrik" sort="B Ckhed, Fredrik" uniqKey="B Ckhed F" first="Fredrik" last="B Ckhed">Fredrik B Ckhed</name><name sortKey="B Ckhed, Fredrik" sort="B Ckhed, Fredrik" uniqKey="B Ckhed F" first="Fredrik" last="B Ckhed">Fredrik B Ckhed</name><name sortKey="B Ckhed, Fredrik" sort="B Ckhed, Fredrik" uniqKey="B Ckhed F" first="Fredrik" last="B Ckhed">Fredrik B Ckhed</name><name sortKey="B Ckhed, Helene Kling" sort="B Ckhed, Helene Kling" uniqKey="B Ckhed H" first="Helene Kling" last="B Ckhed">Helene Kling B Ckhed</name><name sortKey="B Ckhed, Helene Kling" sort="B Ckhed, Helene Kling" uniqKey="B Ckhed H" first="Helene Kling" last="B Ckhed">Helene Kling B Ckhed</name><name sortKey="B Ckhed, Helene Kling" sort="B Ckhed, Helene Kling" uniqKey="B Ckhed H" first="Helene Kling" last="B Ckhed">Helene Kling B Ckhed</name><name sortKey="Caesar, Robert" sort="Caesar, Robert" uniqKey="Caesar R" first="Robert" last="Caesar">Robert Caesar</name><name sortKey="Ketonen, Maria" sort="Ketonen, Maria" uniqKey="Ketonen M" first="Maria" last="Ketonen">Maria Ketonen</name><name sortKey="Ketonen, Maria" sort="Ketonen, Maria" uniqKey="Ketonen M" first="Maria" last="Ketonen">Maria Ketonen</name><name sortKey="Ostergren Lunden, Gunnel" sort="Ostergren Lunden, Gunnel" uniqKey="Ostergren Lunden G" first="Gunnel" last="Östergren Lundén">Gunnel Östergren Lundén</name><name sortKey="Ostergren Lunden, Gunnel" sort="Ostergren Lunden, Gunnel" uniqKey="Ostergren Lunden G" first="Gunnel" last="Östergren Lundén">Gunnel Östergren Lundén</name><name sortKey="Reigstad, Christopher S" sort="Reigstad, Christopher S" uniqKey="Reigstad C" first="Christopher S" last="Reigstad">Christopher S. Reigstad</name><name sortKey="Reigstad, Christopher S" sort="Reigstad, Christopher S" uniqKey="Reigstad C" first="Christopher S" last="Reigstad">Christopher S. Reigstad</name><name sortKey="Reinhardt, Christoph" sort="Reinhardt, Christoph" uniqKey="Reinhardt C" first="Christoph" last="Reinhardt">Christoph Reinhardt</name><name sortKey="Reinhardt, Christoph" sort="Reinhardt, Christoph" uniqKey="Reinhardt C" first="Christoph" last="Reinhardt">Christoph Reinhardt</name></country><country name="Belgique"><region name="Région de Bruxelles-Capitale"><name sortKey="Cani, Patrice D" sort="Cani, Patrice D" uniqKey="Cani P" first="Patrice D" last="Cani">Patrice D. Cani</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Belgique/explor/OpenAccessBelV2/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000803 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 000803 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Belgique
|area= OpenAccessBelV2
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:81B5D4FCEF105E2B57956CC223B59452F03032A2
|texte= Gut-derived lipopolysaccharide augments adipose macrophage accumulation but is not essential for impaired glucose or insulin tolerance in mice
}}
| This area was generated with Dilib version V0.6.25. |  |