T Cell-Mediated Inflammation in Adipose Tissue Does Not Cause Insulin Resistance in Hyperlipidemic Mice
Obesity is associated with chronic inflammation in adipose tissue. Proinflammatory cytokines including tumor necrosis factor-alpha and interleukin-6 secreted by adipose tissue during the metabolic syndrome are proposed to cause local and general insulin resistance and promote development of type 2 d...
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| Veröffentlicht in: | Circulation research 2009-04, Vol.104 (8), p.961-968 |
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| creator | SULTAN, Ariane STRODTHOFF, Daniela ZIERATH, Juleen R ARNER, Peter HANSSON, Goran K ROBERTSON, Anna-Karin PAULSSON-BERNE, Gabrielle FAUCONNIER, Jeremy PARINI, Paolo RYDEN, Mikael THIERRY-MIEG, Nicolas JOHANSSON, Maria E CHIBALIN, Alexander V |
| description | Obesity is associated with chronic inflammation in adipose tissue. Proinflammatory cytokines including tumor necrosis factor-alpha and interleukin-6 secreted by adipose tissue during the metabolic syndrome are proposed to cause local and general insulin resistance and promote development of type 2 diabetes. We have used a compound mutant mouse, Apoe(-/-)xCD4dnTGFbR, with dysregulation of T-cell activation, excessive production of proinflammatory cytokines, hyperlipidemia, and atherosclerosis, to dissect the role of inflammation in adipose tissue metabolism. These mice are lean, which avoids confounding effects of concomitant obesity. Expression and secretion of a set of proinflammatory factors including tumor necrosis factor-alpha, interferon-gamma, and monocyte chemoattractant protein-1 was increased in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice, as was the enzyme 11beta-hydroxysteroid dehydrogenase type 1, which converts cortisone to bioactive cortisol. Interleukin-6, which has an inhibitory glucocorticoid response element in its promoter, was not upregulated. In spite of intense local inflammation, insulin sensitivity was not impaired in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice unless exogenous interleukin-6 was administered. In conclusion, T-cell activation causes inflammation in adipose tissue but does not lead to insulin resistance in this tissue in the absence of interleukin-6. |
| doi_str_mv | 10.1161/CIRCRESAHA.108.190280 |
| format | Article |
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Proinflammatory cytokines including tumor necrosis factor-alpha and interleukin-6 secreted by adipose tissue during the metabolic syndrome are proposed to cause local and general insulin resistance and promote development of type 2 diabetes. We have used a compound mutant mouse, Apoe(-/-)xCD4dnTGFbR, with dysregulation of T-cell activation, excessive production of proinflammatory cytokines, hyperlipidemia, and atherosclerosis, to dissect the role of inflammation in adipose tissue metabolism. These mice are lean, which avoids confounding effects of concomitant obesity. Expression and secretion of a set of proinflammatory factors including tumor necrosis factor-alpha, interferon-gamma, and monocyte chemoattractant protein-1 was increased in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice, as was the enzyme 11beta-hydroxysteroid dehydrogenase type 1, which converts cortisone to bioactive cortisol. Interleukin-6, which has an inhibitory glucocorticoid response element in its promoter, was not upregulated. In spite of intense local inflammation, insulin sensitivity was not impaired in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice unless exogenous interleukin-6 was administered. In conclusion, T-cell activation causes inflammation in adipose tissue but does not lead to insulin resistance in this tissue in the absence of interleukin-6.</description><identifier>ISSN: 0009-7330</identifier><identifier>ISSN: 1524-4571</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/CIRCRESAHA.108.190280</identifier><identifier>PMID: 19299644</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>11-beta-Hydroxysteroid Dehydrogenase Type 1 - metabolism ; Adipokines - metabolism ; Adipose Tissue ; Adipose Tissue, White - immunology ; Adipose Tissue, White - physiopathology ; Animal ; Animals ; Antigens ; Apolipoproteins E - deficiency ; Apolipoproteins E - genetics ; Apolipoproteins E/deficiency/genetics ; Atherosclerosis - genetics ; Atherosclerosis - immunology ; Atherosclerosis - physiopathology ; Atherosclerosis/genetics/immunology/physiopathology ; Biological and medical sciences ; Blood Glucose - metabolism ; Body Weight ; CD4 Antigens - genetics ; CD4-Positive T-Lymphocytes - immunology ; CD4/genetics ; Chemokine CCL2 - metabolism ; Disease Models ; Disease Models, Animal ; Disorders of blood lipids. Hyperlipoproteinemia ; Female ; Fundamental and applied biological sciences. Psychology ; Gene Expression Profiling ; Genetic ; Hydrocortisone - metabolism ; Hyperlipidemias - genetics ; Hyperlipidemias - immunology ; Hyperlipidemias - physiopathology ; Hyperlipidemias/genetics/immunology/physiopathology ; Immunologi inom det medicinska området ; Immunology in the medical area ; Inbred C57BL ; Inflammation - genetics ; Inflammation - immunology ; Inflammation - physiopathology ; Inflammation Mediators - metabolism ; Inflammation/genetics/immunology/physiopathology ; Insulin Resistance ; Interferon-gamma - metabolism ; Interleukin-6 - metabolism ; Knockout ; Lipogenesis ; Medical sciences ; Medicin och hälsovetenskap ; Metabolic diseases ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Promoter Regions ; Promoter Regions, Genetic ; Protein-Serine-Threonine Kinases - genetics ; Receptors ; Receptors, Transforming Growth Factor beta - genetics ; Time Factors ; Transforming Growth Factor beta/genetics ; Transgenic ; Tumor Necrosis Factor-alpha - metabolism ; Vertebrates: cardiovascular system ; White/immunology/physiopathology</subject><ispartof>Circulation research, 2009-04, Vol.104 (8), p.961-968</ispartof><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c477t-492308bed78436868216d581cfed40144fbb7ac73a66e2742435c550c0f6869b3</citedby><cites>FETCH-LOGICAL-c477t-492308bed78436868216d581cfed40144fbb7ac73a66e2742435c550c0f6869b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21431047$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19299644$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/179581$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:118638513$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>SULTAN, Ariane</creatorcontrib><creatorcontrib>STRODTHOFF, Daniela</creatorcontrib><creatorcontrib>ZIERATH, Juleen R</creatorcontrib><creatorcontrib>ARNER, Peter</creatorcontrib><creatorcontrib>HANSSON, Goran K</creatorcontrib><creatorcontrib>ROBERTSON, Anna-Karin</creatorcontrib><creatorcontrib>PAULSSON-BERNE, Gabrielle</creatorcontrib><creatorcontrib>FAUCONNIER, Jeremy</creatorcontrib><creatorcontrib>PARINI, Paolo</creatorcontrib><creatorcontrib>RYDEN, Mikael</creatorcontrib><creatorcontrib>THIERRY-MIEG, Nicolas</creatorcontrib><creatorcontrib>JOHANSSON, Maria E</creatorcontrib><creatorcontrib>CHIBALIN, Alexander V</creatorcontrib><title>T Cell-Mediated Inflammation in Adipose Tissue Does Not Cause Insulin Resistance in Hyperlipidemic Mice</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Obesity is associated with chronic inflammation in adipose tissue. Proinflammatory cytokines including tumor necrosis factor-alpha and interleukin-6 secreted by adipose tissue during the metabolic syndrome are proposed to cause local and general insulin resistance and promote development of type 2 diabetes. We have used a compound mutant mouse, Apoe(-/-)xCD4dnTGFbR, with dysregulation of T-cell activation, excessive production of proinflammatory cytokines, hyperlipidemia, and atherosclerosis, to dissect the role of inflammation in adipose tissue metabolism. These mice are lean, which avoids confounding effects of concomitant obesity. Expression and secretion of a set of proinflammatory factors including tumor necrosis factor-alpha, interferon-gamma, and monocyte chemoattractant protein-1 was increased in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice, as was the enzyme 11beta-hydroxysteroid dehydrogenase type 1, which converts cortisone to bioactive cortisol. Interleukin-6, which has an inhibitory glucocorticoid response element in its promoter, was not upregulated. In spite of intense local inflammation, insulin sensitivity was not impaired in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice unless exogenous interleukin-6 was administered. In conclusion, T-cell activation causes inflammation in adipose tissue but does not lead to insulin resistance in this tissue in the absence of interleukin-6.</description><subject>11-beta-Hydroxysteroid Dehydrogenase Type 1 - metabolism</subject><subject>Adipokines - metabolism</subject><subject>Adipose Tissue</subject><subject>Adipose Tissue, White - immunology</subject><subject>Adipose Tissue, White - physiopathology</subject><subject>Animal</subject><subject>Animals</subject><subject>Antigens</subject><subject>Apolipoproteins E - deficiency</subject><subject>Apolipoproteins E - genetics</subject><subject>Apolipoproteins E/deficiency/genetics</subject><subject>Atherosclerosis - genetics</subject><subject>Atherosclerosis - immunology</subject><subject>Atherosclerosis - physiopathology</subject><subject>Atherosclerosis/genetics/immunology/physiopathology</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Body Weight</subject><subject>CD4 Antigens - genetics</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD4/genetics</subject><subject>Chemokine CCL2 - metabolism</subject><subject>Disease Models</subject><subject>Disease Models, Animal</subject><subject>Disorders of blood lipids. Hyperlipoproteinemia</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Profiling</subject><subject>Genetic</subject><subject>Hydrocortisone - metabolism</subject><subject>Hyperlipidemias - genetics</subject><subject>Hyperlipidemias - immunology</subject><subject>Hyperlipidemias - physiopathology</subject><subject>Hyperlipidemias/genetics/immunology/physiopathology</subject><subject>Immunologi inom det medicinska området</subject><subject>Immunology in the medical area</subject><subject>Inbred C57BL</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Inflammation - physiopathology</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inflammation/genetics/immunology/physiopathology</subject><subject>Insulin Resistance</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-6 - metabolism</subject><subject>Knockout</subject><subject>Lipogenesis</subject><subject>Medical sciences</subject><subject>Medicin och hälsovetenskap</subject><subject>Metabolic diseases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Promoter Regions</subject><subject>Promoter Regions, Genetic</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Receptors</subject><subject>Receptors, Transforming Growth Factor beta - genetics</subject><subject>Time Factors</subject><subject>Transforming Growth Factor beta/genetics</subject><subject>Transgenic</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vertebrates: cardiovascular system</subject><subject>White/immunology/physiopathology</subject><issn>0009-7330</issn><issn>1524-4571</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kktv1DAUhS0EokPhJ4C8gV2mdvxejkJhRmqpNB3WluPcjAx5ESdC_fe4TOis6MrW0XfOtX2M0HtK1pRKelXs9sX--n6z3awp0WtqSK7JC7SiIucZF4q-RCtCiMkUY-QCvYnxByGUs9y8RhfU5MZIzlfoeMAFNE12C1VwE1R419WNa1s3hb7DocObKgx9BHwIMc6AP_cQ8bd-woWbk7rr4twkag8xxMl1Hh4924cBxiYMoYI2eHwbPLxFr2rXRHi3rJfo-5frQ7HNbu6-7orNTea5UlPGTc6ILqFSmjOppc6prISmvoaKp-PzuiyV84o5KSFXPOdMeCGIJ3WiTckuUXbKjb9hmEs7jKF144PtXbCL9DPtwAphiOKJN__lh7GvzqZ_Rkq1ZFpQ9uys4zzYJB3nvxZl0h0S_-nEp-BfM8TJtiH69Pqug36OVioquOYygeIE-rGPcYT6KZoS-9i-PbefJG1P7Sffh2XAXLZQnV1L3Qn4uAAuetfUY2osxCcuT_-DEq7YHx_hubk</recordid><startdate>20090424</startdate><enddate>20090424</enddate><creator>SULTAN, Ariane</creator><creator>STRODTHOFF, Daniela</creator><creator>ZIERATH, Juleen R</creator><creator>ARNER, Peter</creator><creator>HANSSON, Goran K</creator><creator>ROBERTSON, Anna-Karin</creator><creator>PAULSSON-BERNE, Gabrielle</creator><creator>FAUCONNIER, Jeremy</creator><creator>PARINI, Paolo</creator><creator>RYDEN, Mikael</creator><creator>THIERRY-MIEG, Nicolas</creator><creator>JOHANSSON, Maria E</creator><creator>CHIBALIN, Alexander V</creator><general>Lippincott Williams & Wilkins</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>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope></search><sort><creationdate>20090424</creationdate><title>T Cell-Mediated Inflammation in Adipose Tissue Does Not Cause Insulin Resistance in Hyperlipidemic Mice</title><author>SULTAN, Ariane ; STRODTHOFF, Daniela ; ZIERATH, Juleen R ; ARNER, Peter ; HANSSON, Goran K ; ROBERTSON, Anna-Karin ; PAULSSON-BERNE, Gabrielle ; FAUCONNIER, Jeremy ; PARINI, Paolo ; RYDEN, Mikael ; THIERRY-MIEG, Nicolas ; JOHANSSON, Maria E ; CHIBALIN, Alexander V</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c477t-492308bed78436868216d581cfed40144fbb7ac73a66e2742435c550c0f6869b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>11-beta-Hydroxysteroid Dehydrogenase Type 1 - metabolism</topic><topic>Adipokines - metabolism</topic><topic>Adipose Tissue</topic><topic>Adipose Tissue, White - immunology</topic><topic>Adipose Tissue, White - physiopathology</topic><topic>Animal</topic><topic>Animals</topic><topic>Antigens</topic><topic>Apolipoproteins E - deficiency</topic><topic>Apolipoproteins E - genetics</topic><topic>Apolipoproteins E/deficiency/genetics</topic><topic>Atherosclerosis - genetics</topic><topic>Atherosclerosis - immunology</topic><topic>Atherosclerosis - physiopathology</topic><topic>Atherosclerosis/genetics/immunology/physiopathology</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Body Weight</topic><topic>CD4 Antigens - genetics</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD4/genetics</topic><topic>Chemokine CCL2 - metabolism</topic><topic>Disease Models</topic><topic>Disease Models, Animal</topic><topic>Disorders of blood lipids. Hyperlipoproteinemia</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene Expression Profiling</topic><topic>Genetic</topic><topic>Hydrocortisone - metabolism</topic><topic>Hyperlipidemias - genetics</topic><topic>Hyperlipidemias - immunology</topic><topic>Hyperlipidemias - physiopathology</topic><topic>Hyperlipidemias/genetics/immunology/physiopathology</topic><topic>Immunologi inom det medicinska området</topic><topic>Immunology in the medical area</topic><topic>Inbred C57BL</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Inflammation - physiopathology</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inflammation/genetics/immunology/physiopathology</topic><topic>Insulin Resistance</topic><topic>Interferon-gamma - metabolism</topic><topic>Interleukin-6 - metabolism</topic><topic>Knockout</topic><topic>Lipogenesis</topic><topic>Medical sciences</topic><topic>Medicin och hälsovetenskap</topic><topic>Metabolic diseases</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic</topic><topic>Promoter Regions</topic><topic>Promoter Regions, Genetic</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Receptors</topic><topic>Receptors, Transforming Growth Factor beta - genetics</topic><topic>Time Factors</topic><topic>Transforming Growth Factor beta/genetics</topic><topic>Transgenic</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vertebrates: cardiovascular system</topic><topic>White/immunology/physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SULTAN, Ariane</creatorcontrib><creatorcontrib>STRODTHOFF, Daniela</creatorcontrib><creatorcontrib>ZIERATH, Juleen R</creatorcontrib><creatorcontrib>ARNER, Peter</creatorcontrib><creatorcontrib>HANSSON, Goran K</creatorcontrib><creatorcontrib>ROBERTSON, Anna-Karin</creatorcontrib><creatorcontrib>PAULSSON-BERNE, Gabrielle</creatorcontrib><creatorcontrib>FAUCONNIER, Jeremy</creatorcontrib><creatorcontrib>PARINI, Paolo</creatorcontrib><creatorcontrib>RYDEN, Mikael</creatorcontrib><creatorcontrib>THIERRY-MIEG, Nicolas</creatorcontrib><creatorcontrib>JOHANSSON, Maria E</creatorcontrib><creatorcontrib>CHIBALIN, Alexander V</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>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SULTAN, Ariane</au><au>STRODTHOFF, Daniela</au><au>ZIERATH, Juleen R</au><au>ARNER, Peter</au><au>HANSSON, Goran K</au><au>ROBERTSON, Anna-Karin</au><au>PAULSSON-BERNE, Gabrielle</au><au>FAUCONNIER, Jeremy</au><au>PARINI, Paolo</au><au>RYDEN, Mikael</au><au>THIERRY-MIEG, Nicolas</au><au>JOHANSSON, Maria E</au><au>CHIBALIN, Alexander V</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>T Cell-Mediated Inflammation in Adipose Tissue Does Not Cause Insulin Resistance in Hyperlipidemic Mice</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>2009-04-24</date><risdate>2009</risdate><volume>104</volume><issue>8</issue><spage>961</spage><epage>968</epage><pages>961-968</pages><issn>0009-7330</issn><issn>1524-4571</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>Obesity is associated with chronic inflammation in adipose tissue. Proinflammatory cytokines including tumor necrosis factor-alpha and interleukin-6 secreted by adipose tissue during the metabolic syndrome are proposed to cause local and general insulin resistance and promote development of type 2 diabetes. We have used a compound mutant mouse, Apoe(-/-)xCD4dnTGFbR, with dysregulation of T-cell activation, excessive production of proinflammatory cytokines, hyperlipidemia, and atherosclerosis, to dissect the role of inflammation in adipose tissue metabolism. These mice are lean, which avoids confounding effects of concomitant obesity. Expression and secretion of a set of proinflammatory factors including tumor necrosis factor-alpha, interferon-gamma, and monocyte chemoattractant protein-1 was increased in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice, as was the enzyme 11beta-hydroxysteroid dehydrogenase type 1, which converts cortisone to bioactive cortisol. Interleukin-6, which has an inhibitory glucocorticoid response element in its promoter, was not upregulated. In spite of intense local inflammation, insulin sensitivity was not impaired in adipose tissue of Apoe(-/-)xCD4dnTGFbR mice unless exogenous interleukin-6 was administered. In conclusion, T-cell activation causes inflammation in adipose tissue but does not lead to insulin resistance in this tissue in the absence of interleukin-6.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>19299644</pmid><doi>10.1161/CIRCRESAHA.108.190280</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 11-beta-Hydroxysteroid Dehydrogenase Type 1 - metabolism Adipokines - metabolism Adipose Tissue Adipose Tissue, White - immunology Adipose Tissue, White - physiopathology Animal Animals Antigens Apolipoproteins E - deficiency Apolipoproteins E - genetics Apolipoproteins E/deficiency/genetics Atherosclerosis - genetics Atherosclerosis - immunology Atherosclerosis - physiopathology Atherosclerosis/genetics/immunology/physiopathology Biological and medical sciences Blood Glucose - metabolism Body Weight CD4 Antigens - genetics CD4-Positive T-Lymphocytes - immunology CD4/genetics Chemokine CCL2 - metabolism Disease Models Disease Models, Animal Disorders of blood lipids. Hyperlipoproteinemia Female Fundamental and applied biological sciences. Psychology Gene Expression Profiling Genetic Hydrocortisone - metabolism Hyperlipidemias - genetics Hyperlipidemias - immunology Hyperlipidemias - physiopathology Hyperlipidemias/genetics/immunology/physiopathology Immunologi inom det medicinska området Immunology in the medical area Inbred C57BL Inflammation - genetics Inflammation - immunology Inflammation - physiopathology Inflammation Mediators - metabolism Inflammation/genetics/immunology/physiopathology Insulin Resistance Interferon-gamma - metabolism Interleukin-6 - metabolism Knockout Lipogenesis Medical sciences Medicin och hälsovetenskap Metabolic diseases Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Promoter Regions Promoter Regions, Genetic Protein-Serine-Threonine Kinases - genetics Receptors Receptors, Transforming Growth Factor beta - genetics Time Factors Transforming Growth Factor beta/genetics Transgenic Tumor Necrosis Factor-alpha - metabolism Vertebrates: cardiovascular system White/immunology/physiopathology |
| title | T Cell-Mediated Inflammation in Adipose Tissue Does Not Cause Insulin Resistance in Hyperlipidemic Mice |
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