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T cell–mediated hepatic inflammation modulates adiponectin levels in mice: role of tumor necrosis factor α
Experimental T cell–mediated hepatitis induced by concanavalin A (ConA) results in the initiation of an inflammatory response and the production of cytokines. Adiponectin is an adipocytokine produced by adipose tissue that is involved in the reciprocal regulation of other cytokines, including tumor...
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| Published in: | Metabolism, clinical and experimental clinical and experimental, 2006-04, Vol.55 (4), p.555-559 |
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| Main Authors: | , , , , , |
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| Language: | English |
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| cited_by | cdi_FETCH-LOGICAL-c393t-9b8028b9adc086609daa890de3d6a38dce37f20f914a2b1aabf13b7a2e53f0a23 |
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| cites | cdi_FETCH-LOGICAL-c393t-9b8028b9adc086609daa890de3d6a38dce37f20f914a2b1aabf13b7a2e53f0a23 |
| container_end_page | 559 |
| container_issue | 4 |
| container_start_page | 555 |
| container_title | Metabolism, clinical and experimental |
| container_volume | 55 |
| creator | Morris, Alison M. Sennello, Joseph A. Fayad, Raja A. Eckel, Robert H. Dinarello, Charles A. Fantuzzi, Giamila |
| description | Experimental T cell–mediated hepatitis induced by concanavalin A (ConA) results in the initiation of an inflammatory response and the production of cytokines. Adiponectin is an adipocytokine produced by adipose tissue that is involved in the reciprocal regulation of other cytokines, including tumor necrosis factor
α (TNF-
α). Concanavalin A administration to C57BL/6J mice reduced circulating levels of adiponectin, whereas leptin was markedly increased. Adiponectin messenger RNA expression in adipose tissue was also decreased; however, the expression of both the adiponectin receptors remained unchanged. Neutralization of TNF-
α reduced ConA-induced liver damage, and this was associated with restored circulating levels of adiponectin. These findings indicate that inflammation-induced TNF-
α is a critical mediator of adipose-tissue-derived adiponectin in vivo. |
| doi_str_mv | 10.1016/j.metabol.2005.11.008 |
| format | article |
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α (TNF-
α). Concanavalin A administration to C57BL/6J mice reduced circulating levels of adiponectin, whereas leptin was markedly increased. Adiponectin messenger RNA expression in adipose tissue was also decreased; however, the expression of both the adiponectin receptors remained unchanged. Neutralization of TNF-
α reduced ConA-induced liver damage, and this was associated with restored circulating levels of adiponectin. These findings indicate that inflammation-induced TNF-
α is a critical mediator of adipose-tissue-derived adiponectin in vivo.</description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/j.metabol.2005.11.008</identifier><identifier>PMID: 16546488</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adiponectin - blood ; Adiponectin - genetics ; Adipose Tissue - metabolism ; Animals ; Biological and medical sciences ; Concanavalin A ; Hepatitis - blood ; Hepatitis - etiology ; Hepatitis - metabolism ; Hepatitis - pathology ; Leptin - blood ; Medical sciences ; Metabolic diseases ; Mice ; Mice, Inbred C57BL ; Mitogens ; Receptors, Adiponectin ; Receptors, Cell Surface - metabolism ; RNA, Messenger - metabolism ; T-Lymphocytes ; Tumor Necrosis Factor-alpha - antagonists & inhibitors ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Metabolism, clinical and experimental, 2006-04, Vol.55 (4), p.555-559</ispartof><rights>2006 Elsevier Inc.</rights><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-9b8028b9adc086609daa890de3d6a38dce37f20f914a2b1aabf13b7a2e53f0a23</citedby><cites>FETCH-LOGICAL-c393t-9b8028b9adc086609daa890de3d6a38dce37f20f914a2b1aabf13b7a2e53f0a23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17703238$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16546488$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morris, Alison M.</creatorcontrib><creatorcontrib>Sennello, Joseph A.</creatorcontrib><creatorcontrib>Fayad, Raja A.</creatorcontrib><creatorcontrib>Eckel, Robert H.</creatorcontrib><creatorcontrib>Dinarello, Charles A.</creatorcontrib><creatorcontrib>Fantuzzi, Giamila</creatorcontrib><title>T cell–mediated hepatic inflammation modulates adiponectin levels in mice: role of tumor necrosis factor α</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description>Experimental T cell–mediated hepatitis induced by concanavalin A (ConA) results in the initiation of an inflammatory response and the production of cytokines. Adiponectin is an adipocytokine produced by adipose tissue that is involved in the reciprocal regulation of other cytokines, including tumor necrosis factor
α (TNF-
α). Concanavalin A administration to C57BL/6J mice reduced circulating levels of adiponectin, whereas leptin was markedly increased. Adiponectin messenger RNA expression in adipose tissue was also decreased; however, the expression of both the adiponectin receptors remained unchanged. Neutralization of TNF-
α reduced ConA-induced liver damage, and this was associated with restored circulating levels of adiponectin. These findings indicate that inflammation-induced TNF-
α is a critical mediator of adipose-tissue-derived adiponectin in vivo.</description><subject>Adiponectin - blood</subject><subject>Adiponectin - genetics</subject><subject>Adipose Tissue - metabolism</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Concanavalin A</subject><subject>Hepatitis - blood</subject><subject>Hepatitis - etiology</subject><subject>Hepatitis - metabolism</subject><subject>Hepatitis - pathology</subject><subject>Leptin - blood</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mitogens</subject><subject>Receptors, Adiponectin</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>RNA, Messenger - metabolism</subject><subject>T-Lymphocytes</subject><subject>Tumor Necrosis Factor-alpha - antagonists & inhibitors</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqFkU1u1TAQgC0Eoq-FI4C8gV3COE4chw1CFX9SJTZlbU38I_xkx484qdQdd-AkXIRDcBIcvUhdshqP5hvP-DMhLxjUDJh4c6yjXXBMoW4AupqxGkA-IgfW8aaSAuAxOQA0ooJ26C7IZc5HAOh7KZ6SCya6VrRSHki8pdqG8Pfnr2iNx8Ua-t2ecPGa-skFjLGc00RjMmso5UzR-FOarF78RIO9syEXkkav7Vs6p2BpcnRZY5ppgeaUfaYO9VLyP7-fkScOQ7bP93hFvn38cHv9ubr5-unL9fubSvOBL9UwSmjkOKDRIIWAwSDKAYzlRiCXRlveuwbcwFpsRoY4OsbHHhvbcQfY8Cvy-nzvaU4_VpsXFX3e3omTTWtWou9F2_Ub2J3BbdM8W6dOs4843ysGavOsjmr3rDbPijFVPJe-l_uAdSziHrp2sQV4tQOYNQY346R9fuD6HnjDN-7dmSse7Z23s8ra20mXz5iLY2WS_88q_wARW6IJ</recordid><startdate>20060401</startdate><enddate>20060401</enddate><creator>Morris, Alison M.</creator><creator>Sennello, Joseph A.</creator><creator>Fayad, Raja A.</creator><creator>Eckel, Robert H.</creator><creator>Dinarello, Charles A.</creator><creator>Fantuzzi, Giamila</creator><general>Elsevier Inc</general><general>Elsevier</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></search><sort><creationdate>20060401</creationdate><title>T cell–mediated hepatic inflammation modulates adiponectin levels in mice: role of tumor necrosis factor α</title><author>Morris, Alison M. ; Sennello, Joseph A. ; Fayad, Raja A. ; Eckel, Robert H. ; Dinarello, Charles A. ; Fantuzzi, Giamila</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-9b8028b9adc086609daa890de3d6a38dce37f20f914a2b1aabf13b7a2e53f0a23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adiponectin - blood</topic><topic>Adiponectin - genetics</topic><topic>Adipose Tissue - metabolism</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Concanavalin A</topic><topic>Hepatitis - blood</topic><topic>Hepatitis - etiology</topic><topic>Hepatitis - metabolism</topic><topic>Hepatitis - pathology</topic><topic>Leptin - blood</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mitogens</topic><topic>Receptors, Adiponectin</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>RNA, Messenger - metabolism</topic><topic>T-Lymphocytes</topic><topic>Tumor Necrosis Factor-alpha - antagonists & inhibitors</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morris, Alison M.</creatorcontrib><creatorcontrib>Sennello, Joseph A.</creatorcontrib><creatorcontrib>Fayad, Raja A.</creatorcontrib><creatorcontrib>Eckel, Robert H.</creatorcontrib><creatorcontrib>Dinarello, Charles A.</creatorcontrib><creatorcontrib>Fantuzzi, Giamila</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><jtitle>Metabolism, clinical and experimental</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morris, Alison M.</au><au>Sennello, Joseph A.</au><au>Fayad, Raja A.</au><au>Eckel, Robert H.</au><au>Dinarello, Charles A.</au><au>Fantuzzi, Giamila</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>T cell–mediated hepatic inflammation modulates adiponectin levels in mice: role of tumor necrosis factor α</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>2006-04-01</date><risdate>2006</risdate><volume>55</volume><issue>4</issue><spage>555</spage><epage>559</epage><pages>555-559</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract>Experimental T cell–mediated hepatitis induced by concanavalin A (ConA) results in the initiation of an inflammatory response and the production of cytokines. Adiponectin is an adipocytokine produced by adipose tissue that is involved in the reciprocal regulation of other cytokines, including tumor necrosis factor
α (TNF-
α). Concanavalin A administration to C57BL/6J mice reduced circulating levels of adiponectin, whereas leptin was markedly increased. Adiponectin messenger RNA expression in adipose tissue was also decreased; however, the expression of both the adiponectin receptors remained unchanged. Neutralization of TNF-
α reduced ConA-induced liver damage, and this was associated with restored circulating levels of adiponectin. These findings indicate that inflammation-induced TNF-
α is a critical mediator of adipose-tissue-derived adiponectin in vivo.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>16546488</pmid><doi>10.1016/j.metabol.2005.11.008</doi><tpages>5</tpages></addata></record> |
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| ispartof | Metabolism, clinical and experimental, 2006-04, Vol.55 (4), p.555-559 |
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| language | eng |
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| subjects | Adiponectin - blood Adiponectin - genetics Adipose Tissue - metabolism Animals Biological and medical sciences Concanavalin A Hepatitis - blood Hepatitis - etiology Hepatitis - metabolism Hepatitis - pathology Leptin - blood Medical sciences Metabolic diseases Mice Mice, Inbred C57BL Mitogens Receptors, Adiponectin Receptors, Cell Surface - metabolism RNA, Messenger - metabolism T-Lymphocytes Tumor Necrosis Factor-alpha - antagonists & inhibitors Tumor Necrosis Factor-alpha - metabolism |
| title | T cell–mediated hepatic inflammation modulates adiponectin levels in mice: role of tumor necrosis factor α |
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