Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance.
Identifieur interne : 000D65 ( Main/Exploration ); précédent : 000D64; suivant : 000D66Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance.
Auteurs : T. Sano [Japon] ; S. Nagayasu [Japon] ; S. Suzuki [Japon] ; M. Iwashita [Japon] ; A. Yamashita [Japon] ; T. Shinjo [Japon] ; T. Sanui [Japon] ; A. Kushiyama [Japon] ; T. Kanematsu [Japon] ; T. Asano [Japon] ; F. Nishimura [Japon]Source :
- Nutrition, metabolism, and cardiovascular diseases : NMCD [ 1590-3729 ] ; 2017.
Descripteurs français
- KwdFr :
- Activation des macrophages (effets des médicaments et des substances chimiques), Adipocytes (effets des médicaments et des substances chimiques), Adipocytes (métabolisme), Alimentation riche en graisse (effets indésirables), Animaux (MeSH), Anti-inflammatoires (pharmacologie), Catéchine (pharmacologie), Cellules 3T3-L1 (MeSH), Cellules RAW 264.7 (MeSH), Chimiokine CCL19 (génétique), Chimiokine CCL19 (métabolisme), Facteurs temps (MeSH), Insulinorésistance (MeSH), Macrophages (effets des médicaments et des substances chimiques), Macrophages (métabolisme), Modèles animaux de maladie humaine (MeSH), Obésité (génétique), Obésité (métabolisme), Obésité (prévention et contrôle), Obésité (étiologie), Panniculite (génétique), Panniculite (métabolisme), Panniculite (prévention et contrôle), Panniculite (étiologie), Régulation négative (MeSH), Souris (MeSH), Souris de lignée C57BL (MeSH), Techniques de coculture (MeSH), Tissu adipeux (effets des médicaments et des substances chimiques), Tissu adipeux (métabolisme).
- MESH :
- effets des médicaments et des substances chimiques : Activation des macrophages, Adipocytes, Macrophages, Tissu adipeux.
- effets indésirables : Alimentation riche en graisse.
- génétique : Chimiokine CCL19, Obésité, Panniculite.
- métabolisme : Adipocytes, Chimiokine CCL19, Macrophages, Obésité, Panniculite, Tissu adipeux.
- pharmacologie : Anti-inflammatoires, Catéchine.
- prévention et contrôle : Obésité, Panniculite.
- étiologie : Obésité, Panniculite.
- Animaux, Cellules 3T3-L1, Cellules RAW 264.7, Facteurs temps, Insulinorésistance, Modèles animaux de maladie humaine, Régulation négative, Souris, Souris de lignée C57BL, Techniques de coculture.
English descriptors
- KwdEn :
- 3T3-L1 Cells (MeSH), Adipocytes (drug effects), Adipocytes (metabolism), Adipose Tissue (drug effects), Adipose Tissue (metabolism), Animals (MeSH), Anti-Inflammatory Agents (pharmacology), Catechin (pharmacology), Chemokine CCL19 (genetics), Chemokine CCL19 (metabolism), Coculture Techniques (MeSH), Diet, High-Fat (adverse effects), Disease Models, Animal (MeSH), Down-Regulation (MeSH), Insulin Resistance (MeSH), Macrophage Activation (drug effects), Macrophages (drug effects), Macrophages (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Obesity (etiology), Obesity (genetics), Obesity (metabolism), Obesity (prevention & control), Panniculitis (etiology), Panniculitis (genetics), Panniculitis (metabolism), Panniculitis (prevention & control), RAW 264.7 Cells (MeSH), Time Factors (MeSH).
- MESH :
- chemical , genetics : Chemokine CCL19.
- chemical , metabolism : Chemokine CCL19.
- chemical , pharmacology : Anti-Inflammatory Agents, Catechin.
- adverse effects : Diet, High-Fat.
- drug effects : Adipocytes, Adipose Tissue, Macrophage Activation, Macrophages.
- etiology : Obesity, Panniculitis.
- genetics : Obesity, Panniculitis.
- metabolism : Adipocytes, Adipose Tissue, Macrophages, Obesity, Panniculitis.
- prevention & control : Obesity, Panniculitis.
- 3T3-L1 Cells, Animals, Coculture Techniques, Disease Models, Animal, Down-Regulation, Insulin Resistance, Mice, Mice, Inbred C57BL, RAW 264.7 Cells, Time Factors.
Abstract
BACKGROUND AND AIMS
Epicatechin (EC) intake has been suggested to be beneficial for the prevention of cardiovascular disorders, and it is well known that adipose tissue inflammation is one of the major risk factors for coronary heart diseases. The purpose of the present study was to determine the in vitro and in vivo effects of EC on adipose tissue inflammation and obesity.
METHODS AND RESULTS
DNA microarray analysis was performed to evaluate the effects of EC on gene expression in adipocytes co-cultured with bacterial endotoxin-stimulated macrophages. To determine the in vivo effects of the catechin, C57BL/6 mice were fed either a high-fat diet (HFD) or HFD combined with EC, and metabolic changes were observed EC suppressed the expression of many inflammatory genes in the adipocytes co-cultured with endotoxin-stimulated macrophages. Specifically, EC markedly suppressed chemokine (CC motif) ligand 19 (CCL19) expression. The target cell of EC appeared to macrophages. The in vivo study indicated that mice fed the EC-supplemented HFD were protected from diet-induced obesity and insulin resistance. Accordingly, the expression levels of genes associated with inflammation in adipose tissue and in the liver were downregulated in this group of mice.
CONCLUSIONS
EC exerts beneficial effects for the prevention of adipose tissue inflammation and insulin resistance. Since we previously reported that mice deficient in the CCL19 receptor were protected from diet-induced obesity and insulin resistance, it can be concluded that the beneficial effects of EC could be mediated, at least in part, by marked suppression of CCL19 expression.
DOI: 10.1016/j.numecd.2016.11.008
PubMed: 28062181
Affiliations:
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Le document en format XML
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Sano</name><affiliation wicri:level="1"><nlm:affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka</wicri:regionArea><wicri:noRegion>Fukuoka</wicri:noRegion></affiliation></author><author><name sortKey="Nagayasu, S" sort="Nagayasu, S" uniqKey="Nagayasu S" first="S" last="Nagayasu">S. Nagayasu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Dental Science for Health Promotion, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Dental Science for Health Promotion, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Suzuki, S" sort="Suzuki, S" uniqKey="Suzuki S" first="S" last="Suzuki">S. 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Shinjo</name><affiliation wicri:level="1"><nlm:affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka</wicri:regionArea><wicri:noRegion>Fukuoka</wicri:noRegion></affiliation></author><author><name sortKey="Sanui, T" sort="Sanui, T" uniqKey="Sanui T" first="T" last="Sanui">T. Sanui</name><affiliation wicri:level="1"><nlm:affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka</wicri:regionArea><wicri:noRegion>Fukuoka</wicri:noRegion></affiliation></author><author><name sortKey="Kushiyama, A" sort="Kushiyama, A" uniqKey="Kushiyama A" first="A" last="Kushiyama">A. Kushiyama</name><affiliation wicri:level="3"><nlm:affiliation>Division of Metabolic Diseases, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Division of Metabolic Diseases, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo</wicri:regionArea><placeName><settlement type="city">Tokyo</settlement><region type="région">Région de Kantō</region></placeName></affiliation></author><author><name sortKey="Kanematsu, T" sort="Kanematsu, T" uniqKey="Kanematsu T" first="T" last="Kanematsu">T. Kanematsu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Cellular and Molecular Pharmacology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Cellular and Molecular Pharmacology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Asano, T" sort="Asano, T" uniqKey="Asano T" first="T" last="Asano">T. Asano</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biological Chemistry, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Biological Chemistry, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima</wicri:regionArea><wicri:noRegion>Hiroshima</wicri:noRegion></affiliation></author><author><name sortKey="Nishimura, F" sort="Nishimura, F" uniqKey="Nishimura F" first="F" last="Nishimura">F. Nishimura</name><affiliation wicri:level="1"><nlm:affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan. Electronic address: fusanori@dent.kyushu-u.ac.jp.</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka</wicri:regionArea><wicri:noRegion>Fukuoka</wicri:noRegion></affiliation></author></analytic><series><title level="j">Nutrition, metabolism, and cardiovascular diseases : NMCD</title><idno type="eISSN">1590-3729</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>3T3-L1 Cells (MeSH)</term><term>Adipocytes (drug effects)</term><term>Adipocytes (metabolism)</term><term>Adipose Tissue (drug effects)</term><term>Adipose Tissue (metabolism)</term><term>Animals (MeSH)</term><term>Anti-Inflammatory Agents (pharmacology)</term><term>Catechin (pharmacology)</term><term>Chemokine CCL19 (genetics)</term><term>Chemokine CCL19 (metabolism)</term><term>Coculture Techniques (MeSH)</term><term>Diet, High-Fat (adverse effects)</term><term>Disease Models, Animal (MeSH)</term><term>Down-Regulation (MeSH)</term><term>Insulin Resistance (MeSH)</term><term>Macrophage Activation (drug effects)</term><term>Macrophages (drug effects)</term><term>Macrophages (metabolism)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Obesity (etiology)</term><term>Obesity (genetics)</term><term>Obesity (metabolism)</term><term>Obesity (prevention & control)</term><term>Panniculitis (etiology)</term><term>Panniculitis (genetics)</term><term>Panniculitis (metabolism)</term><term>Panniculitis (prevention & control)</term><term>RAW 264.7 Cells (MeSH)</term><term>Time Factors (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation des macrophages (effets des médicaments et des substances chimiques)</term><term>Adipocytes (effets des médicaments et des substances chimiques)</term><term>Adipocytes (métabolisme)</term><term>Alimentation riche en graisse (effets indésirables)</term><term>Animaux (MeSH)</term><term>Anti-inflammatoires (pharmacologie)</term><term>Catéchine (pharmacologie)</term><term>Cellules 3T3-L1 (MeSH)</term><term>Cellules RAW 264.7 (MeSH)</term><term>Chimiokine CCL19 (génétique)</term><term>Chimiokine CCL19 (métabolisme)</term><term>Facteurs temps (MeSH)</term><term>Insulinorésistance (MeSH)</term><term>Macrophages (effets des médicaments et des substances chimiques)</term><term>Macrophages (métabolisme)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Obésité (génétique)</term><term>Obésité (métabolisme)</term><term>Obésité (prévention et contrôle)</term><term>Obésité (étiologie)</term><term>Panniculite (génétique)</term><term>Panniculite (métabolisme)</term><term>Panniculite (prévention et contrôle)</term><term>Panniculite (étiologie)</term><term>Régulation négative (MeSH)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Techniques de coculture (MeSH)</term><term>Tissu adipeux (effets des médicaments et des substances chimiques)</term><term>Tissu adipeux (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Chemokine CCL19</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Chemokine CCL19</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>Catechin</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Diet, High-Fat</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Adipocytes</term><term>Adipose Tissue</term><term>Macrophage Activation</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Activation des macrophages</term><term>Adipocytes</term><term>Macrophages</term><term>Tissu adipeux</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Alimentation riche en graisse</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Obesity</term><term>Panniculitis</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Obesity</term><term>Panniculitis</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Chimiokine CCL19</term><term>Obésité</term><term>Panniculite</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Adipocytes</term><term>Adipose Tissue</term><term>Macrophages</term><term>Obesity</term><term>Panniculitis</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Adipocytes</term><term>Chimiokine CCL19</term><term>Macrophages</term><term>Obésité</term><term>Panniculite</term><term>Tissu adipeux</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term><term>Catéchine</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Obesity</term><term>Panniculitis</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Obésité</term><term>Panniculite</term></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Obésité</term><term>Panniculite</term></keywords><keywords scheme="MESH" xml:lang="en"><term>3T3-L1 Cells</term><term>Animals</term><term>Coculture Techniques</term><term>Disease Models, Animal</term><term>Down-Regulation</term><term>Insulin Resistance</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>RAW 264.7 Cells</term><term>Time Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules 3T3-L1</term><term>Cellules RAW 264.7</term><term>Facteurs temps</term><term>Insulinorésistance</term><term>Modèles animaux de maladie humaine</term><term>Régulation négative</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Techniques de coculture</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND AND AIMS</b></p><p>Epicatechin (EC) intake has been suggested to be beneficial for the prevention of cardiovascular disorders, and it is well known that adipose tissue inflammation is one of the major risk factors for coronary heart diseases. The purpose of the present study was to determine the in vitro and in vivo effects of EC on adipose tissue inflammation and obesity.</p></div><div type="abstract" xml:lang="en"><p><b>METHODS AND RESULTS</b></p><p>DNA microarray analysis was performed to evaluate the effects of EC on gene expression in adipocytes co-cultured with bacterial endotoxin-stimulated macrophages. To determine the in vivo effects of the catechin, C57BL/6 mice were fed either a high-fat diet (HFD) or HFD combined with EC, and metabolic changes were observed EC suppressed the expression of many inflammatory genes in the adipocytes co-cultured with endotoxin-stimulated macrophages. Specifically, EC markedly suppressed chemokine (CC motif) ligand 19 (CCL19) expression. The target cell of EC appeared to macrophages. The in vivo study indicated that mice fed the EC-supplemented HFD were protected from diet-induced obesity and insulin resistance. Accordingly, the expression levels of genes associated with inflammation in adipose tissue and in the liver were downregulated in this group of mice.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>EC exerts beneficial effects for the prevention of adipose tissue inflammation and insulin resistance. Since we previously reported that mice deficient in the CCL19 receptor were protected from diet-induced obesity and insulin resistance, it can be concluded that the beneficial effects of EC could be mediated, at least in part, by marked suppression of CCL19 expression.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28062181</PMID><DateCompleted><Year>2017</Year><Month>09</Month><Day>05</Day></DateCompleted><DateRevised><Year>2017</Year><Month>09</Month><Day>06</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1590-3729</ISSN><JournalIssue CitedMedium="Internet"><Volume>27</Volume><Issue>3</Issue><PubDate><Year>2017</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Nutrition, metabolism, and cardiovascular diseases : NMCD</Title><ISOAbbreviation>Nutr Metab Cardiovasc Dis</ISOAbbreviation></Journal><ArticleTitle>Epicatechin downregulates adipose tissue CCL19 expression and thereby ameliorates diet-induced obesity and insulin resistance.</ArticleTitle><Pagination><MedlinePgn>249-259</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0939-4753(16)30200-9</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.numecd.2016.11.008</ELocationID><Abstract><AbstractText Label="BACKGROUND AND AIMS" NlmCategory="OBJECTIVE">Epicatechin (EC) intake has been suggested to be beneficial for the prevention of cardiovascular disorders, and it is well known that adipose tissue inflammation is one of the major risk factors for coronary heart diseases. The purpose of the present study was to determine the in vitro and in vivo effects of EC on adipose tissue inflammation and obesity.</AbstractText><AbstractText Label="METHODS AND RESULTS" NlmCategory="RESULTS">DNA microarray analysis was performed to evaluate the effects of EC on gene expression in adipocytes co-cultured with bacterial endotoxin-stimulated macrophages. To determine the in vivo effects of the catechin, C57BL/6 mice were fed either a high-fat diet (HFD) or HFD combined with EC, and metabolic changes were observed EC suppressed the expression of many inflammatory genes in the adipocytes co-cultured with endotoxin-stimulated macrophages. Specifically, EC markedly suppressed chemokine (CC motif) ligand 19 (CCL19) expression. The target cell of EC appeared to macrophages. The in vivo study indicated that mice fed the EC-supplemented HFD were protected from diet-induced obesity and insulin resistance. Accordingly, the expression levels of genes associated with inflammation in adipose tissue and in the liver were downregulated in this group of mice.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">EC exerts beneficial effects for the prevention of adipose tissue inflammation and insulin resistance. Since we previously reported that mice deficient in the CCL19 receptor were protected from diet-induced obesity and insulin resistance, it can be concluded that the beneficial effects of EC could be mediated, at least in part, by marked suppression of CCL19 expression.</AbstractText><CopyrightInformation>Copyright © 2016 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II University. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sano</LastName><ForeName>T</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nagayasu</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Dental Science for Health Promotion, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Suzuki</LastName><ForeName>S</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Dental Science for Health Promotion, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Iwashita</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yamashita</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shinjo</LastName><ForeName>T</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sanui</LastName><ForeName>T</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kushiyama</LastName><ForeName>A</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Division of Metabolic Diseases, The Institute for Adult Diseases, Asahi Life Foundation, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kanematsu</LastName><ForeName>T</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Cellular and Molecular Pharmacology, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Asano</LastName><ForeName>T</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Biological Chemistry, Hiroshima University Institute of Biomedical and Health Sciences, Hiroshima, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nishimura</LastName><ForeName>F</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Section of Periodontology, Kyushu University Faculty of Dental Science, Fukuoka, Japan. Electronic address: fusanori@dent.kyushu-u.ac.jp.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>11</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Nutr Metab Cardiovasc Dis</MedlineTA><NlmUniqueID>9111474</NlmUniqueID><ISSNLinking>0939-4753</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C515461">Ccl19 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054415">Chemokine CCL19</NameOfSubstance></Chemical><Chemical><RegistryNumber>8R1V1STN48</RegistryNumber><NameOfSubstance UI="D002392">Catechin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D041721" MajorTopicYN="N">3T3-L1 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017667" MajorTopicYN="N">Adipocytes</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000273" MajorTopicYN="N">Adipose Tissue</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002392" MajorTopicYN="N">Catechin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054415" MajorTopicYN="N">Chemokine CCL19</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018920" MajorTopicYN="N">Coculture Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D059305" MajorTopicYN="N">Diet, High-Fat</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="Y">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015536" MajorTopicYN="N">Down-Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007333" MajorTopicYN="Y">Insulin Resistance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008262" MajorTopicYN="N">Macrophage Activation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009765" MajorTopicYN="N">Obesity</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015434" MajorTopicYN="N">Panniculitis</DescriptorName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000067996" MajorTopicYN="N">RAW 264.7 Cells</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Adipocyte–macrophage interaction</Keyword><Keyword MajorTopicYN="N">Adipokine</Keyword><Keyword MajorTopicYN="N">CCL19</Keyword><Keyword MajorTopicYN="N">Epicatechin</Keyword><Keyword MajorTopicYN="N">Inflammation</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2016</Year><Month>08</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2016</Year><Month>11</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2016</Year><Month>11</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>1</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>9</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>1</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28062181</ArticleId><ArticleId IdType="pii">S0939-4753(16)30200-9</ArticleId><ArticleId IdType="doi">10.1016/j.numecd.2016.11.008</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Japon</li></country><region><li>Région de Kantō</li></region><settlement><li>Tokyo</li></settlement></list><tree><country name="Japon"><noRegion><name sortKey="Sano, T" sort="Sano, T" uniqKey="Sano T" first="T" last="Sano">T. Sano</name></noRegion><name sortKey="Asano, T" sort="Asano, T" uniqKey="Asano T" first="T" last="Asano">T. Asano</name><name sortKey="Iwashita, M" sort="Iwashita, M" uniqKey="Iwashita M" first="M" last="Iwashita">M. Iwashita</name><name sortKey="Kanematsu, T" sort="Kanematsu, T" uniqKey="Kanematsu T" first="T" last="Kanematsu">T. Kanematsu</name><name sortKey="Kushiyama, A" sort="Kushiyama, A" uniqKey="Kushiyama A" first="A" last="Kushiyama">A. Kushiyama</name><name sortKey="Nagayasu, S" sort="Nagayasu, S" uniqKey="Nagayasu S" first="S" last="Nagayasu">S. Nagayasu</name><name sortKey="Nishimura, F" sort="Nishimura, F" uniqKey="Nishimura F" first="F" last="Nishimura">F. Nishimura</name><name sortKey="Sanui, T" sort="Sanui, T" uniqKey="Sanui T" first="T" last="Sanui">T. Sanui</name><name sortKey="Shinjo, T" sort="Shinjo, T" uniqKey="Shinjo T" first="T" last="Shinjo">T. Shinjo</name><name sortKey="Suzuki, S" sort="Suzuki, S" uniqKey="Suzuki S" first="S" last="Suzuki">S. Suzuki</name><name sortKey="Yamashita, A" sort="Yamashita, A" uniqKey="Yamashita A" first="A" last="Yamashita">A. Yamashita</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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