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<publisher>HAL CCSD</publisher>
<title lang=en>Indomethacin treatment prevents high fat diet-induced obesity and insulin resistance but not glucose intolerance in C57BL/6J mice.</title>
<creator>Fjære, Even</creator>
<creator>Aune, Ulrike L</creator>
<creator>Røen, Kristin</creator>
<creator>Keenan, Alison H</creator>
<creator>Ma, Tao</creator>
<creator>Borkowski, Kamil</creator>
<creator>Kristensen, David M</creator>
<creator>Novotny, Guy W</creator>
<creator>Mandrup-Poulsen, Thomas</creator>
<creator>Hudson, Brian D</creator>
<creator>Milligan, Graeme</creator>
<creator>Xi, Yannan</creator>
<creator>Newman, John W</creator>
<creator>Haj, Fawaz G</creator>
<creator>Liaset, Bjørn</creator>
<creator>Kristiansen, Karsten</creator>
<creator>Madsen, Lise</creator>
<contributor>University of Bergen (UIB)</contributor>
<contributor>University of Copenhagen (KU)</contributor>
<contributor>Universite de Californie</contributor>
<contributor>Institut de recherche, santé, environnement et travail [Rennes] (Irset) ; Université d'Angers (UA) - Université des Antilles et de la Guyane (UAG) - Université de Rennes 1 (UR1) - École des Hautes Études en Santé Publique [EHESP] (EHESP) - Institut National de la Santé et de la Recherche Médicale (INSERM) - Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )</contributor>
<contributor>Department of Biology ; University of Copenhagen (KU)</contributor>
<contributor>Stockholm University</contributor>
<contributor>Molecular Pharmacology Group ; University of Glasgow - College of Medical, Veterinary and Life Sciences</contributor>
<contributor>We thank Trond Ulven for providing TUG469. We would also thank Pavel Flachs and Jan Kopecky for kindly providing the UCP1 antibody. This work was supported by the EU FP7 project DIABAT (HEALTH-F2-2011-278373), the Danish Natural Science Research Council, the Novo Nordisk Foundation, the Carlsberg Foundation, the SHARE Cross Faculty PhD Initiative of University of Copenhagen and NIFES. Part of the work was carried out as a part of the research program of the Danish Obesity Research Centre (DanORC). DanORC is supported by the Danish Council for Strategic Research (Grant No: 2101 06 0005). Part of the work was also supported by the Danish Council for Strategic Research (grant 11-116196 for the FFARMED project). The F.G.H laboratory receives funding from Juvenile Diabetes Research Foundation (1-2009-337) and NIH (RO1DK090492). This study was supported in part by intramural funds from the USDA Agricultural Research Service [5306-51000-002-00D to JWN; 5306-51000-019-00D to JWN] and the National Institute of Food and Agriculture National Needs Fellowship [2008-38420-04759 to AHK].</contributor>
<description>International audience</description>
<source>ISSN: 0021-9258</source>
<source>EISSN: 1083-351X</source>
<source>Journal of Biological Chemistry</source>
<publisher>American Society for Biochemistry and Molecular Biology</publisher>
<identifier>hal-01074835</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01074835</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01074835/document</identifier>
<identifier>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01074835/file/JBC-2013-525220v2-Kristiansen-POSTPRINT.pdf</identifier>
<source>https://hal-univ-rennes1.archives-ouvertes.fr/hal-01074835</source>
<source>Journal of Biological Chemistry, American Society for Biochemistry and Molecular Biology, 2014, 289 (23), pp.16032-45. 〈10.1074/jbc.M113.525220〉</source>
<identifier>DOI : 10.1074/jbc.M113.525220</identifier>
<relation>info:eu-repo/semantics/altIdentifier/doi/10.1074/jbc.M113.525220</relation>
<identifier>PUBMED : 24742673</identifier>
<relation>info:eu-repo/semantics/altIdentifier/pmid/24742673</relation>
<language>en</language>
<subject lang=en>Glucose intolerance Cyclooxygenase inhibitors</subject>
<subject lang=en>Insulin secretion</subject>
<subject lang=en>Insulin resistance receptors (GPCR)</subject>
<subject lang=en>G protein coupled</subject>
<subject lang=en>Cyclooxygenase (COX) pathway Adipose tissue</subject>
<subject>[SDV] Life Sciences [q-bio]</subject>
<type>info:eu-repo/semantics/article</type>
<type>Journal articles</type>
<description lang=en>Chronic low grade inflammation is closely linked to obesity-associated insulin resistance. To examine how administration of the anti-inflammatory compound indomethacin, a general cyclooxygenase inhibitor, affected obesity development and insulin sensitivity, we fed obesity-prone male C57BL/6J mice a high fat/high sucrose (HF/HS) diet or a regular diet supplemented or not with indomethacin (±INDO) for 7 weeks. Development of obesity, insulin resistance, and glucose intolerance was monitored, and the effect of indomethacin on glucose-stimulated insulin secretion (GSIS) was measured in vivo and in vitro using MIN6 β-cells. We found that supplementation with indomethacin prevented HF/HS-induced obesity and diet-induced changes in systemic insulin sensitivity. Thus, HF/HS+INDO-fed mice remained insulin-sensitive. However, mice fed HF/HS+INDO exhibited pronounced glucose intolerance. Hepatic glucose output was significantly increased. Indomethacin had no effect on adipose tissue mass, glucose tolerance, or GSIS when included in a regular diet. Indomethacin administration to obese mice did not reduce adipose tissue mass, and the compensatory increase in GSIS observed in obese mice was not affected by treatment with indomethacin. We demonstrate that indomethacin did not inhibit GSIS per se, but activation of GPR40 in the presence of indomethacin inhibited glucose-dependent insulin secretion in MIN6 cells. We conclude that constitutive high hepatic glucose output combined with impaired GSIS in response to activation of GPR40-dependent signaling in the HF/HS+INDO-fed mice contributed to the impaired glucose clearance during a glucose challenge and that the resulting lower levels of plasma insulin prevented the obesogenic action of the HF/HS diet.</description>
<date>2014-06-06</date>
<contributor>European Project : 278373, EC:FP7:HEALTH, FP7-HEALTH-2011-two-stage, DIABAT(2011)</contributor>
<relation>info:eu-repo/grantAgreement/EC/FP7/278373/EU/Recruitment and activation of brown adipocytes as preventive and curative therapy for type 2 diabetes/DIABAT</relation>
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