Nutritional Supplementation With trans-10, cis-12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue
Nutritional Supplementation With trans -10, cis -12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue Hélène Poirier 1 , Jennifer S. Shapiro 2 , Roy J. Kim 2 and Mitchell A. Lazar 2 1 Physiologie de la Nutrition, Ecole Nationale Supérieure de Biologie Appliquée á la Nutrition et...
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| Veröffentlicht in: | Diabetes (New York, N.Y.) N.Y.), 2006-06, Vol.55 (6), p.1634-1641 |
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| creator | POIRIER, Hélène SHAPIRO, Jennifer S KIM, Roy J LAZAR, Mitchell A |
| description | Nutritional Supplementation With trans -10, cis -12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue
Hélène Poirier 1 ,
Jennifer S. Shapiro 2 ,
Roy J. Kim 2 and
Mitchell A. Lazar 2
1 Physiologie de la Nutrition, Ecole Nationale Supérieure de Biologie Appliquée á la Nutrition et á l’Alimentation (ENSBANA),
Unité Mixte de Recherche 5170 Centre Européen des Sciences du Goût (CESG)-Centre National de la Recherche Scientifique/Institut
National de la Recherche Agronomique/Université de Bourgogne, Dijon, France
2 Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine, Genetics, and Pharmacology, and The Institute
for Diabetes, Obesity, and Metabolism, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Address correspondence and reprint requests to Helene Poirier, PhD, Physiologie de la Nutrition, ENSBANA, Unité Mixte de Recherche
5170 CESG–Centre National de la Recherche Scientifique/Institut National de la Recherche Agronomique/Université de Bourgogne,
Dijon, 21000 France. E-mail: hpoirier{at}u-bourgogne.fr
Abstract
Conjugated linoleic acids (CLAs) are conjugated dienoic isomers of linoleic acid. Many people supplement their diets with
CLAs to attempt weight loss, and the trans -10, cis -12 isomer ( t10 , c12 -CLA) of CLA reduces adiposity in animal models and humans. However, CLA treatment in mice causes insulin resistance that
has been attributed to the lipoatrophic state, which is associated with hyperinsulinemia and hepatic steatosis. Here, we investigated
the effect of t10 , c12 -CLA on adipose tissue inflammation, another factor promoting insulin resistance. We confirmed that t10 , c12 -CLA daily gavage performed in mice reduces white adipose tissue (WAT) mass and adiponectin and leptin serum levels and provokes
hyperinsulinemia. In parallel, we demonstrated that this CLA isomer led to a rapid induction of inflammatory factors such
as tumor necrosis factor-α and interleukin-6 gene expression in WAT without affecting their serum levels. In vitro, t10 , c12 -CLA directly induced IL-6 secretion in 3T3-L1 adipocytes by an nuclear factor-κB–dependent mechanism. In vivo, however, the
lipoatrophic adipose tissue of CLA-treated mice was notable for a dramatic increase in macrophage infiltration and gene expression.
Thus, CLA supplementation directly induces inflammatory gene expression in adipocytes and also promotes macrophage infiltration
into adipose tissue to a local inflammatory state that con |
| doi_str_mv | 10.2337/db06-0036 |
| format | Article |
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Hélène Poirier 1 ,
Jennifer S. Shapiro 2 ,
Roy J. Kim 2 and
Mitchell A. Lazar 2
1 Physiologie de la Nutrition, Ecole Nationale Supérieure de Biologie Appliquée á la Nutrition et á l’Alimentation (ENSBANA),
Unité Mixte de Recherche 5170 Centre Européen des Sciences du Goût (CESG)-Centre National de la Recherche Scientifique/Institut
National de la Recherche Agronomique/Université de Bourgogne, Dijon, France
2 Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine, Genetics, and Pharmacology, and The Institute
for Diabetes, Obesity, and Metabolism, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Address correspondence and reprint requests to Helene Poirier, PhD, Physiologie de la Nutrition, ENSBANA, Unité Mixte de Recherche
5170 CESG–Centre National de la Recherche Scientifique/Institut National de la Recherche Agronomique/Université de Bourgogne,
Dijon, 21000 France. E-mail: hpoirier{at}u-bourgogne.fr
Abstract
Conjugated linoleic acids (CLAs) are conjugated dienoic isomers of linoleic acid. Many people supplement their diets with
CLAs to attempt weight loss, and the trans -10, cis -12 isomer ( t10 , c12 -CLA) of CLA reduces adiposity in animal models and humans. However, CLA treatment in mice causes insulin resistance that
has been attributed to the lipoatrophic state, which is associated with hyperinsulinemia and hepatic steatosis. Here, we investigated
the effect of t10 , c12 -CLA on adipose tissue inflammation, another factor promoting insulin resistance. We confirmed that t10 , c12 -CLA daily gavage performed in mice reduces white adipose tissue (WAT) mass and adiponectin and leptin serum levels and provokes
hyperinsulinemia. In parallel, we demonstrated that this CLA isomer led to a rapid induction of inflammatory factors such
as tumor necrosis factor-α and interleukin-6 gene expression in WAT without affecting their serum levels. In vitro, t10 , c12 -CLA directly induced IL-6 secretion in 3T3-L1 adipocytes by an nuclear factor-κB–dependent mechanism. In vivo, however, the
lipoatrophic adipose tissue of CLA-treated mice was notable for a dramatic increase in macrophage infiltration and gene expression.
Thus, CLA supplementation directly induces inflammatory gene expression in adipocytes and also promotes macrophage infiltration
into adipose tissue to a local inflammatory state that contributes to insulin resistance.
c9,t11-CLA, cis-9,trans-11 isomer of conjugated linoleic acid
CLA, conjugated linoleic acid
DMEM, Dulbecco’s modified Eagle’s medium
FBS, fetal bovine serum
IRβ, insulin receptor β
IRS-1, insulin receptor substrate 1
IL-6, interleukin-6
MCP-1, monocyte chemoattractant protein-1
NF-κB, nuclear factor-κB
PAI-1, plasminogen activator inhibitor-1
PPAR, peroxisome proliferator–activated receptor
SOCS3, suppressors of cytokine signaling 3
t10,c12-CLA, trans-10,cis-12 isomer of conjugated linoleic acid
TNF-α, tumor necrosis factor-α
WAT, white adipose tissue
Footnotes
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted March 6, 2006.
Received January 7, 2006.
DIABETES</description><identifier>ISSN: 0012-1797</identifier><identifier>EISSN: 1939-327X</identifier><identifier>DOI: 10.2337/db06-0036</identifier><identifier>PMID: 16731825</identifier><identifier>CODEN: DIAEAZ</identifier><language>eng</language><publisher>Alexandria, VA: American Diabetes Association</publisher><subject>3T3-L1 Cells ; Adiponectin - blood ; Adipose tissue ; Adipose Tissue, White - drug effects ; Adipose Tissue, White - metabolism ; Adipose Tissue, White - pathology ; Adipose tissues ; Animals ; Biological and medical sciences ; Body fat ; Diabetes. Impaired glucose tolerance ; Dietary Supplements ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Enzyme-Linked Immunosorbent Assay ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Food and Nutrition ; Health aspects ; Hyperinsulinism - blood ; Hyperinsulinism - chemically induced ; Immunohistochemistry ; Inflammation - blood ; Inflammation - chemically induced ; Insulin Resistance ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Laboratories ; Leptin - blood ; Life Sciences ; Linoleic acid ; Linoleic acids ; Linoleic Acids, Conjugated - administration & dosage ; Linoleic Acids, Conjugated - pharmacology ; Macrophages - metabolism ; Macrophages - pathology ; Medical sciences ; Mice ; Mice, Inbred C57BL ; NF-kappa B - metabolism ; Overweight persons ; PPAR gamma - metabolism ; Resistin - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF</subject><ispartof>Diabetes (New York, N.Y.), 2006-06, Vol.55 (6), p.1634-1641</ispartof><rights>2006 INIST-CNRS</rights><rights>COPYRIGHT 2006 American Diabetes Association</rights><rights>COPYRIGHT 2006 American Diabetes Association</rights><rights>Copyright American Diabetes Association Jun 2006</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-66b4e30499937ec7149485f807cbc70ad64e44e9f8815ca289b46a58bc7f34493</citedby><cites>FETCH-LOGICAL-c474t-66b4e30499937ec7149485f807cbc70ad64e44e9f8815ca289b46a58bc7f34493</cites><orcidid>0000-0001-8055-1571</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17820952$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16731825$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://institut-agro-dijon.hal.science/hal-01915822$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>POIRIER, Hélène</creatorcontrib><creatorcontrib>SHAPIRO, Jennifer S</creatorcontrib><creatorcontrib>KIM, Roy J</creatorcontrib><creatorcontrib>LAZAR, Mitchell A</creatorcontrib><title>Nutritional Supplementation With trans-10, cis-12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue</title><title>Diabetes (New York, N.Y.)</title><addtitle>Diabetes</addtitle><description>Nutritional Supplementation With trans -10, cis -12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue
Hélène Poirier 1 ,
Jennifer S. Shapiro 2 ,
Roy J. Kim 2 and
Mitchell A. Lazar 2
1 Physiologie de la Nutrition, Ecole Nationale Supérieure de Biologie Appliquée á la Nutrition et á l’Alimentation (ENSBANA),
Unité Mixte de Recherche 5170 Centre Européen des Sciences du Goût (CESG)-Centre National de la Recherche Scientifique/Institut
National de la Recherche Agronomique/Université de Bourgogne, Dijon, France
2 Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine, Genetics, and Pharmacology, and The Institute
for Diabetes, Obesity, and Metabolism, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Address correspondence and reprint requests to Helene Poirier, PhD, Physiologie de la Nutrition, ENSBANA, Unité Mixte de Recherche
5170 CESG–Centre National de la Recherche Scientifique/Institut National de la Recherche Agronomique/Université de Bourgogne,
Dijon, 21000 France. E-mail: hpoirier{at}u-bourgogne.fr
Abstract
Conjugated linoleic acids (CLAs) are conjugated dienoic isomers of linoleic acid. Many people supplement their diets with
CLAs to attempt weight loss, and the trans -10, cis -12 isomer ( t10 , c12 -CLA) of CLA reduces adiposity in animal models and humans. However, CLA treatment in mice causes insulin resistance that
has been attributed to the lipoatrophic state, which is associated with hyperinsulinemia and hepatic steatosis. Here, we investigated
the effect of t10 , c12 -CLA on adipose tissue inflammation, another factor promoting insulin resistance. We confirmed that t10 , c12 -CLA daily gavage performed in mice reduces white adipose tissue (WAT) mass and adiponectin and leptin serum levels and provokes
hyperinsulinemia. In parallel, we demonstrated that this CLA isomer led to a rapid induction of inflammatory factors such
as tumor necrosis factor-α and interleukin-6 gene expression in WAT without affecting their serum levels. In vitro, t10 , c12 -CLA directly induced IL-6 secretion in 3T3-L1 adipocytes by an nuclear factor-κB–dependent mechanism. In vivo, however, the
lipoatrophic adipose tissue of CLA-treated mice was notable for a dramatic increase in macrophage infiltration and gene expression.
Thus, CLA supplementation directly induces inflammatory gene expression in adipocytes and also promotes macrophage infiltration
into adipose tissue to a local inflammatory state that contributes to insulin resistance.
c9,t11-CLA, cis-9,trans-11 isomer of conjugated linoleic acid
CLA, conjugated linoleic acid
DMEM, Dulbecco’s modified Eagle’s medium
FBS, fetal bovine serum
IRβ, insulin receptor β
IRS-1, insulin receptor substrate 1
IL-6, interleukin-6
MCP-1, monocyte chemoattractant protein-1
NF-κB, nuclear factor-κB
PAI-1, plasminogen activator inhibitor-1
PPAR, peroxisome proliferator–activated receptor
SOCS3, suppressors of cytokine signaling 3
t10,c12-CLA, trans-10,cis-12 isomer of conjugated linoleic acid
TNF-α, tumor necrosis factor-α
WAT, white adipose tissue
Footnotes
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted March 6, 2006.
Received January 7, 2006.
DIABETES</description><subject>3T3-L1 Cells</subject><subject>Adiponectin - blood</subject><subject>Adipose tissue</subject><subject>Adipose Tissue, White - drug effects</subject><subject>Adipose Tissue, White - metabolism</subject><subject>Adipose Tissue, White - pathology</subject><subject>Adipose tissues</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Body fat</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Dietary Supplements</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Food and Nutrition</subject><subject>Health aspects</subject><subject>Hyperinsulinism - blood</subject><subject>Hyperinsulinism - chemically induced</subject><subject>Immunohistochemistry</subject><subject>Inflammation - blood</subject><subject>Inflammation - chemically induced</subject><subject>Insulin Resistance</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Laboratories</subject><subject>Leptin - blood</subject><subject>Life Sciences</subject><subject>Linoleic acid</subject><subject>Linoleic acids</subject><subject>Linoleic Acids, Conjugated - administration & dosage</subject><subject>Linoleic Acids, Conjugated - pharmacology</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-kappa B - metabolism</subject><subject>Overweight persons</subject><subject>PPAR gamma - metabolism</subject><subject>Resistin - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><issn>0012-1797</issn><issn>1939-327X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptks1u1DAUhSMEokNhwQugCIlFBSn-Sxwvo1FpK43ogqKysxznJuOREw-xA-2Od-ANeRIcZsSo0ugurnX9-dg6PknyGqNzQin_2NSoyBCixZNkgQUVGSX829NkgRAmGeaCnyQvvN8ghIpYz5MTXHCKS5IvkofPUxhNMG5QNv0ybbcWehiCmifpnQnrNIxq8BlGH1JtYid_fv1eumEzdSpAk67M4CwYnVbaNOn10EwafOytVX2_U3Fterc2AdKqMVvnIb013k_wMnnWKuvh1b6fJl8_Xdwur7LVzeX1slplmnEWsqKoGVDEhBCUg-aYCVbmbYm4rjVHqikYMAaiLUuca0VKUbNC5WXcbCljgp4mZzvdtbJyO5pejQ_SKSOvqpWcZwgLnJeE_MCRfbtjt6P7PoEPcuOmMVrjJcEFi5fyGcp2UKcsSDO0LlqkOxhgVNYN0Jo4rjDjBFH87wHnR_hYDfRGHz1w9uhAZALch05N3svycvWYzY6x2lkLHcjo5PLmqLYenfcjtP8twUjOYZJzmOQcpsi-2bsx1T00B3Kfngi82wPKa2XbmJSYkQPHS4JETiL3fv8Fplv_NCPIxqgaAvjDIs9lEZUpo38Bs2rckw</recordid><startdate>200606</startdate><enddate>200606</enddate><creator>POIRIER, Hélène</creator><creator>SHAPIRO, Jennifer S</creator><creator>KIM, Roy J</creator><creator>LAZAR, Mitchell A</creator><general>American Diabetes Association</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>8GL</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BEC</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HCIFZ</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M2P</scope><scope>M7P</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0001-8055-1571</orcidid></search><sort><creationdate>200606</creationdate><title>Nutritional Supplementation With trans-10, cis-12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue</title><author>POIRIER, Hélène ; SHAPIRO, Jennifer S ; KIM, Roy J ; LAZAR, Mitchell A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-66b4e30499937ec7149485f807cbc70ad64e44e9f8815ca289b46a58bc7f34493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>3T3-L1 Cells</topic><topic>Adiponectin - blood</topic><topic>Adipose tissue</topic><topic>Adipose Tissue, White - drug effects</topic><topic>Adipose Tissue, White - metabolism</topic><topic>Adipose Tissue, White - pathology</topic><topic>Adipose tissues</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Body fat</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Dietary Supplements</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Food and Nutrition</topic><topic>Health aspects</topic><topic>Hyperinsulinism - blood</topic><topic>Hyperinsulinism - chemically induced</topic><topic>Immunohistochemistry</topic><topic>Inflammation - blood</topic><topic>Inflammation - chemically induced</topic><topic>Insulin Resistance</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Laboratories</topic><topic>Leptin - blood</topic><topic>Life Sciences</topic><topic>Linoleic acid</topic><topic>Linoleic acids</topic><topic>Linoleic Acids, Conjugated - administration & dosage</topic><topic>Linoleic Acids, Conjugated - pharmacology</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-kappa B - metabolism</topic><topic>Overweight persons</topic><topic>PPAR gamma - metabolism</topic><topic>Resistin - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>POIRIER, Hélène</creatorcontrib><creatorcontrib>SHAPIRO, Jennifer S</creatorcontrib><creatorcontrib>KIM, Roy J</creatorcontrib><creatorcontrib>LAZAR, Mitchell A</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: High School</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>eLibrary</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>SciTech Premium Collection</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Diabetes (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>POIRIER, Hélène</au><au>SHAPIRO, Jennifer S</au><au>KIM, Roy J</au><au>LAZAR, Mitchell A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nutritional Supplementation With trans-10, cis-12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue</atitle><jtitle>Diabetes (New York, N.Y.)</jtitle><addtitle>Diabetes</addtitle><date>2006-06</date><risdate>2006</risdate><volume>55</volume><issue>6</issue><spage>1634</spage><epage>1641</epage><pages>1634-1641</pages><issn>0012-1797</issn><eissn>1939-327X</eissn><coden>DIAEAZ</coden><abstract>Nutritional Supplementation With trans -10, cis -12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue
Hélène Poirier 1 ,
Jennifer S. Shapiro 2 ,
Roy J. Kim 2 and
Mitchell A. Lazar 2
1 Physiologie de la Nutrition, Ecole Nationale Supérieure de Biologie Appliquée á la Nutrition et á l’Alimentation (ENSBANA),
Unité Mixte de Recherche 5170 Centre Européen des Sciences du Goût (CESG)-Centre National de la Recherche Scientifique/Institut
National de la Recherche Agronomique/Université de Bourgogne, Dijon, France
2 Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine, Genetics, and Pharmacology, and The Institute
for Diabetes, Obesity, and Metabolism, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania
Address correspondence and reprint requests to Helene Poirier, PhD, Physiologie de la Nutrition, ENSBANA, Unité Mixte de Recherche
5170 CESG–Centre National de la Recherche Scientifique/Institut National de la Recherche Agronomique/Université de Bourgogne,
Dijon, 21000 France. E-mail: hpoirier{at}u-bourgogne.fr
Abstract
Conjugated linoleic acids (CLAs) are conjugated dienoic isomers of linoleic acid. Many people supplement their diets with
CLAs to attempt weight loss, and the trans -10, cis -12 isomer ( t10 , c12 -CLA) of CLA reduces adiposity in animal models and humans. However, CLA treatment in mice causes insulin resistance that
has been attributed to the lipoatrophic state, which is associated with hyperinsulinemia and hepatic steatosis. Here, we investigated
the effect of t10 , c12 -CLA on adipose tissue inflammation, another factor promoting insulin resistance. We confirmed that t10 , c12 -CLA daily gavage performed in mice reduces white adipose tissue (WAT) mass and adiponectin and leptin serum levels and provokes
hyperinsulinemia. In parallel, we demonstrated that this CLA isomer led to a rapid induction of inflammatory factors such
as tumor necrosis factor-α and interleukin-6 gene expression in WAT without affecting their serum levels. In vitro, t10 , c12 -CLA directly induced IL-6 secretion in 3T3-L1 adipocytes by an nuclear factor-κB–dependent mechanism. In vivo, however, the
lipoatrophic adipose tissue of CLA-treated mice was notable for a dramatic increase in macrophage infiltration and gene expression.
Thus, CLA supplementation directly induces inflammatory gene expression in adipocytes and also promotes macrophage infiltration
into adipose tissue to a local inflammatory state that contributes to insulin resistance.
c9,t11-CLA, cis-9,trans-11 isomer of conjugated linoleic acid
CLA, conjugated linoleic acid
DMEM, Dulbecco’s modified Eagle’s medium
FBS, fetal bovine serum
IRβ, insulin receptor β
IRS-1, insulin receptor substrate 1
IL-6, interleukin-6
MCP-1, monocyte chemoattractant protein-1
NF-κB, nuclear factor-κB
PAI-1, plasminogen activator inhibitor-1
PPAR, peroxisome proliferator–activated receptor
SOCS3, suppressors of cytokine signaling 3
t10,c12-CLA, trans-10,cis-12 isomer of conjugated linoleic acid
TNF-α, tumor necrosis factor-α
WAT, white adipose tissue
Footnotes
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore
be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Accepted March 6, 2006.
Received January 7, 2006.
DIABETES</abstract><cop>Alexandria, VA</cop><pub>American Diabetes Association</pub><pmid>16731825</pmid><doi>10.2337/db06-0036</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0001-8055-1571</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0012-1797 |
| ispartof | Diabetes (New York, N.Y.), 2006-06, Vol.55 (6), p.1634-1641 |
| issn | 0012-1797 1939-327X |
| language | eng |
| recordid | cdi_hal_primary_oai_HAL_hal_01915822v1 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | 3T3-L1 Cells Adiponectin - blood Adipose tissue Adipose Tissue, White - drug effects Adipose Tissue, White - metabolism Adipose Tissue, White - pathology Adipose tissues Animals Biological and medical sciences Body fat Diabetes. Impaired glucose tolerance Dietary Supplements Endocrine pancreas. Apud cells (diseases) Endocrinopathies Enzyme-Linked Immunosorbent Assay Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Food and Nutrition Health aspects Hyperinsulinism - blood Hyperinsulinism - chemically induced Immunohistochemistry Inflammation - blood Inflammation - chemically induced Insulin Resistance Interleukin-6 - genetics Interleukin-6 - metabolism Laboratories Leptin - blood Life Sciences Linoleic acid Linoleic acids Linoleic Acids, Conjugated - administration & dosage Linoleic Acids, Conjugated - pharmacology Macrophages - metabolism Macrophages - pathology Medical sciences Mice Mice, Inbred C57BL NF-kappa B - metabolism Overweight persons PPAR gamma - metabolism Resistin - metabolism Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF |
| title | Nutritional Supplementation With trans-10, cis-12–Conjugated Linoleic Acid Induces Inflammation of White Adipose Tissue |
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