Sympathetic Nerve Activity Maintains an Anti-Inflammatory State in Adipose Tissue in Male Mice by Inhibiting TNF-α Gene Expression in Macrophages
Adipose tissue macrophages (ATMs) play an important role in the inflammatory response in obese animals. How ATMs are regulated in lean animals has remained elusive, however. We now show that the sympathetic nervous system (SNS) is necessary to maintain the abundance of the mRNA for the proinflammato...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2015-10, Vol.156 (10), p.3680-3694 |
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| creator | Tang, Lijun Okamoto, Shiki Shiuchi, Tetsuya Toda, Chitoku Takagi, Kazuyo Sato, Tatsuya Saito, Kumiko Yokota, Shigefumi Minokoshi, Yasuhiko |
| description | Adipose tissue macrophages (ATMs) play an important role in the inflammatory response in obese animals. How ATMs are regulated in lean animals has remained elusive, however. We now show that the sympathetic nervous system (SNS) is necessary to maintain the abundance of the mRNA for the proinflammatory cytokine TNF-α at a low level in ATMs of lean mice. Intracerebroventricular injection of agouti-related neuropeptide increased the amount of TNF-α mRNA in epididymal (epi) white adipose tissue (WAT), but not in interscapular brown adipose tissue (BAT), through inhibition of sympathetic nerve activity in epiWAT. The surgical denervation and β-adrenergic antagonist propranolol up-regulated TNF-α mRNA in both epiWAT and BAT in vivo. Signaling by the β2-adrenergic receptor (AR) and protein kinase A down-regulated TNF-α mRNA in epiWAT explants and suppressed lipopolysaccharide-induced up-regulation of TNF-α mRNA in the stromal vascular fraction of this tissue. β-AR-deficient (β-less) mice manifested an increased plasma TNF-α concentration and increased TNF-α mRNA abundance in epiWAT and BAT. TNF-α mRNA abundance was greater in ATMs (CD11b+ cells of the stromal vascular fraction) from epiWAT or BAT of wild-type mice than in corresponding CD11b− cells, and β2-AR mRNA abundance was greater in ATMs than in CD11b− cells of epiWAT. Our results show that the SNS and β2-AR-protein kinase A pathway maintain an anti-inflammatory state in ATMs of lean mice in vivo, and that the brain melanocortin pathway plays a role in maintaining this state in WAT of lean mice via the SNS. |
| doi_str_mv | 10.1210/EN.2015-1096 |
| format | Article |
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How ATMs are regulated in lean animals has remained elusive, however. We now show that the sympathetic nervous system (SNS) is necessary to maintain the abundance of the mRNA for the proinflammatory cytokine TNF-α at a low level in ATMs of lean mice. Intracerebroventricular injection of agouti-related neuropeptide increased the amount of TNF-α mRNA in epididymal (epi) white adipose tissue (WAT), but not in interscapular brown adipose tissue (BAT), through inhibition of sympathetic nerve activity in epiWAT. The surgical denervation and β-adrenergic antagonist propranolol up-regulated TNF-α mRNA in both epiWAT and BAT in vivo. Signaling by the β2-adrenergic receptor (AR) and protein kinase A down-regulated TNF-α mRNA in epiWAT explants and suppressed lipopolysaccharide-induced up-regulation of TNF-α mRNA in the stromal vascular fraction of this tissue. β-AR-deficient (β-less) mice manifested an increased plasma TNF-α concentration and increased TNF-α mRNA abundance in epiWAT and BAT. TNF-α mRNA abundance was greater in ATMs (CD11b+ cells of the stromal vascular fraction) from epiWAT or BAT of wild-type mice than in corresponding CD11b− cells, and β2-AR mRNA abundance was greater in ATMs than in CD11b− cells of epiWAT. Our results show that the SNS and β2-AR-protein kinase A pathway maintain an anti-inflammatory state in ATMs of lean mice in vivo, and that the brain melanocortin pathway plays a role in maintaining this state in WAT of lean mice via the SNS.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/EN.2015-1096</identifier><identifier>PMID: 26132918</identifier><language>eng</language><publisher>United States: Endocrine Society</publisher><subject>Abundance ; Adipose tissue ; Adipose tissue (brown) ; Adipose Tissue, Brown - drug effects ; Adipose Tissue, Brown - innervation ; Adipose Tissue, Brown - metabolism ; Adipose Tissue, White - drug effects ; Adipose Tissue, White - innervation ; Adipose Tissue, White - metabolism ; Adrenergic beta-Antagonists - pharmacology ; Adrenergic receptors ; Agouti-Related Protein - administration & dosage ; Animals ; Body fat ; CD11b antigen ; Cell Line ; Denervation ; Epididymis - drug effects ; Epididymis - metabolism ; Explants ; Gene expression ; Gene Expression - drug effects ; Immunoblotting ; Inflammation ; Inflammation Mediators - metabolism ; Inflammatory response ; Injections, Intraventricular ; Intracerebroventricular administration ; Kinases ; Lipopolysaccharides ; Low level ; Macrophages ; Macrophages - metabolism ; Male ; Melanocortin ; Mice, Inbred C57BL ; Mice, Knockout ; Nerves ; Peptide Fragments - administration & dosage ; Propranolol ; Propranolol - pharmacology ; Protein kinase A ; Proteins ; Receptors (physiology) ; Receptors, Adrenergic, beta - genetics ; Receptors, Adrenergic, beta - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Sympathectomy ; Sympathetic nerves ; Sympathetic nervous system ; Sympathetic Nervous System - metabolism ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-α</subject><ispartof>Endocrinology (Philadelphia), 2015-10, Vol.156 (10), p.3680-3694</ispartof><rights>Copyright © 2015 by the Endocrine Society</rights><rights>Copyright © 2015 by the Endocrine Society 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-827b3e8b6920576675e892d6bd2078bacf561ef62f5cfb43f91fa94a09782ba63</citedby><cites>FETCH-LOGICAL-c476t-827b3e8b6920576675e892d6bd2078bacf561ef62f5cfb43f91fa94a09782ba63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26132918$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, Lijun</creatorcontrib><creatorcontrib>Okamoto, Shiki</creatorcontrib><creatorcontrib>Shiuchi, Tetsuya</creatorcontrib><creatorcontrib>Toda, Chitoku</creatorcontrib><creatorcontrib>Takagi, Kazuyo</creatorcontrib><creatorcontrib>Sato, Tatsuya</creatorcontrib><creatorcontrib>Saito, Kumiko</creatorcontrib><creatorcontrib>Yokota, Shigefumi</creatorcontrib><creatorcontrib>Minokoshi, Yasuhiko</creatorcontrib><title>Sympathetic Nerve Activity Maintains an Anti-Inflammatory State in Adipose Tissue in Male Mice by Inhibiting TNF-α Gene Expression in Macrophages</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Adipose tissue macrophages (ATMs) play an important role in the inflammatory response in obese animals. How ATMs are regulated in lean animals has remained elusive, however. We now show that the sympathetic nervous system (SNS) is necessary to maintain the abundance of the mRNA for the proinflammatory cytokine TNF-α at a low level in ATMs of lean mice. Intracerebroventricular injection of agouti-related neuropeptide increased the amount of TNF-α mRNA in epididymal (epi) white adipose tissue (WAT), but not in interscapular brown adipose tissue (BAT), through inhibition of sympathetic nerve activity in epiWAT. The surgical denervation and β-adrenergic antagonist propranolol up-regulated TNF-α mRNA in both epiWAT and BAT in vivo. Signaling by the β2-adrenergic receptor (AR) and protein kinase A down-regulated TNF-α mRNA in epiWAT explants and suppressed lipopolysaccharide-induced up-regulation of TNF-α mRNA in the stromal vascular fraction of this tissue. β-AR-deficient (β-less) mice manifested an increased plasma TNF-α concentration and increased TNF-α mRNA abundance in epiWAT and BAT. TNF-α mRNA abundance was greater in ATMs (CD11b+ cells of the stromal vascular fraction) from epiWAT or BAT of wild-type mice than in corresponding CD11b− cells, and β2-AR mRNA abundance was greater in ATMs than in CD11b− cells of epiWAT. Our results show that the SNS and β2-AR-protein kinase A pathway maintain an anti-inflammatory state in ATMs of lean mice in vivo, and that the brain melanocortin pathway plays a role in maintaining this state in WAT of lean mice via the SNS.</description><subject>Abundance</subject><subject>Adipose tissue</subject><subject>Adipose tissue (brown)</subject><subject>Adipose Tissue, Brown - drug effects</subject><subject>Adipose Tissue, Brown - innervation</subject><subject>Adipose Tissue, Brown - metabolism</subject><subject>Adipose Tissue, White - drug effects</subject><subject>Adipose Tissue, White - innervation</subject><subject>Adipose Tissue, White - metabolism</subject><subject>Adrenergic beta-Antagonists - pharmacology</subject><subject>Adrenergic receptors</subject><subject>Agouti-Related Protein - administration & dosage</subject><subject>Animals</subject><subject>Body fat</subject><subject>CD11b antigen</subject><subject>Cell Line</subject><subject>Denervation</subject><subject>Epididymis - drug effects</subject><subject>Epididymis - metabolism</subject><subject>Explants</subject><subject>Gene expression</subject><subject>Gene Expression - drug effects</subject><subject>Immunoblotting</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inflammatory response</subject><subject>Injections, Intraventricular</subject><subject>Intracerebroventricular administration</subject><subject>Kinases</subject><subject>Lipopolysaccharides</subject><subject>Low level</subject><subject>Macrophages</subject><subject>Macrophages - metabolism</subject><subject>Male</subject><subject>Melanocortin</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nerves</subject><subject>Peptide Fragments - administration & dosage</subject><subject>Propranolol</subject><subject>Propranolol - pharmacology</subject><subject>Protein kinase A</subject><subject>Proteins</subject><subject>Receptors (physiology)</subject><subject>Receptors, Adrenergic, beta - genetics</subject><subject>Receptors, Adrenergic, beta - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Sympathectomy</subject><subject>Sympathetic nerves</subject><subject>Sympathetic nervous system</subject><subject>Sympathetic Nervous System - metabolism</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-α</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kc1u1DAUhS0EotPCjjWyxKIsSPFPYsfLUTUtI3WGRYd15CQ3HVeJE2ynIq_Bm_AifSY8zQASgoVl-frz0fE5CL2h5IIySj6utheM0CyhRIlnaEFVmiWSSvIcLQihPJGMyRN06v19PKZpyl-iEyYoZ4rmC_T9duoGHfYQTIW34B4AL6tgHkyY8EYbG-LyWFu8tMEka9u0uut06N2Eb4MOgE28qs3Qe8A74_34NNnoFvDGVIDLCa_t3pQmGHuHd9ur5PEHvgYLePVtcOC96e38onL9sNd34F-hF41uPbw-7mfoy9Vqd_kpufl8vb5c3iRVKkVIciZLDnkpFCOZFEJmkCtWi7JmROalrppMUGgEa7KqKVPeKNpolWqiZM5KLfgZej_rDq7_OoIPRWd8BW2rLfSjL6ikXMW8VBbRd3-h9_3obHRXcMqJJGlMOVIfZip-xXsHTTE402k3FZQUh66K1bY4dFUcuor426PoWHZQ_4Z_lROB8xnox-F_UslRis8k2LqvnLHwlO0fl_808BNJRKvb</recordid><startdate>201510</startdate><enddate>201510</enddate><creator>Tang, Lijun</creator><creator>Okamoto, Shiki</creator><creator>Shiuchi, Tetsuya</creator><creator>Toda, Chitoku</creator><creator>Takagi, Kazuyo</creator><creator>Sato, Tatsuya</creator><creator>Saito, Kumiko</creator><creator>Yokota, Shigefumi</creator><creator>Minokoshi, Yasuhiko</creator><general>Endocrine Society</general><general>Oxford University Press</general><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>7QG</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>201510</creationdate><title>Sympathetic Nerve Activity Maintains an Anti-Inflammatory State in Adipose Tissue in Male Mice by Inhibiting TNF-α Gene Expression in Macrophages</title><author>Tang, Lijun ; Okamoto, Shiki ; Shiuchi, Tetsuya ; Toda, Chitoku ; Takagi, Kazuyo ; Sato, Tatsuya ; Saito, Kumiko ; Yokota, Shigefumi ; Minokoshi, Yasuhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-827b3e8b6920576675e892d6bd2078bacf561ef62f5cfb43f91fa94a09782ba63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Abundance</topic><topic>Adipose tissue</topic><topic>Adipose tissue (brown)</topic><topic>Adipose Tissue, Brown - drug effects</topic><topic>Adipose Tissue, Brown - innervation</topic><topic>Adipose Tissue, Brown - metabolism</topic><topic>Adipose Tissue, White - drug effects</topic><topic>Adipose Tissue, White - innervation</topic><topic>Adipose Tissue, White - metabolism</topic><topic>Adrenergic beta-Antagonists - pharmacology</topic><topic>Adrenergic receptors</topic><topic>Agouti-Related Protein - administration & dosage</topic><topic>Animals</topic><topic>Body fat</topic><topic>CD11b antigen</topic><topic>Cell Line</topic><topic>Denervation</topic><topic>Epididymis - drug effects</topic><topic>Epididymis - metabolism</topic><topic>Explants</topic><topic>Gene expression</topic><topic>Gene Expression - drug effects</topic><topic>Immunoblotting</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inflammatory response</topic><topic>Injections, Intraventricular</topic><topic>Intracerebroventricular administration</topic><topic>Kinases</topic><topic>Lipopolysaccharides</topic><topic>Low level</topic><topic>Macrophages</topic><topic>Macrophages - metabolism</topic><topic>Male</topic><topic>Melanocortin</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Nerves</topic><topic>Peptide Fragments - administration & dosage</topic><topic>Propranolol</topic><topic>Propranolol - pharmacology</topic><topic>Protein kinase A</topic><topic>Proteins</topic><topic>Receptors (physiology)</topic><topic>Receptors, Adrenergic, beta - genetics</topic><topic>Receptors, Adrenergic, beta - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Sympathectomy</topic><topic>Sympathetic nerves</topic><topic>Sympathetic nervous system</topic><topic>Sympathetic Nervous System - metabolism</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, Lijun</creatorcontrib><creatorcontrib>Okamoto, Shiki</creatorcontrib><creatorcontrib>Shiuchi, Tetsuya</creatorcontrib><creatorcontrib>Toda, Chitoku</creatorcontrib><creatorcontrib>Takagi, Kazuyo</creatorcontrib><creatorcontrib>Sato, Tatsuya</creatorcontrib><creatorcontrib>Saito, Kumiko</creatorcontrib><creatorcontrib>Yokota, Shigefumi</creatorcontrib><creatorcontrib>Minokoshi, Yasuhiko</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Animal Behavior Abstracts</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Endocrinology (Philadelphia)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, Lijun</au><au>Okamoto, Shiki</au><au>Shiuchi, Tetsuya</au><au>Toda, Chitoku</au><au>Takagi, Kazuyo</au><au>Sato, Tatsuya</au><au>Saito, Kumiko</au><au>Yokota, Shigefumi</au><au>Minokoshi, Yasuhiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sympathetic Nerve Activity Maintains an Anti-Inflammatory State in Adipose Tissue in Male Mice by Inhibiting TNF-α Gene Expression in Macrophages</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2015-10</date><risdate>2015</risdate><volume>156</volume><issue>10</issue><spage>3680</spage><epage>3694</epage><pages>3680-3694</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><abstract>Adipose tissue macrophages (ATMs) play an important role in the inflammatory response in obese animals. How ATMs are regulated in lean animals has remained elusive, however. We now show that the sympathetic nervous system (SNS) is necessary to maintain the abundance of the mRNA for the proinflammatory cytokine TNF-α at a low level in ATMs of lean mice. Intracerebroventricular injection of agouti-related neuropeptide increased the amount of TNF-α mRNA in epididymal (epi) white adipose tissue (WAT), but not in interscapular brown adipose tissue (BAT), through inhibition of sympathetic nerve activity in epiWAT. The surgical denervation and β-adrenergic antagonist propranolol up-regulated TNF-α mRNA in both epiWAT and BAT in vivo. Signaling by the β2-adrenergic receptor (AR) and protein kinase A down-regulated TNF-α mRNA in epiWAT explants and suppressed lipopolysaccharide-induced up-regulation of TNF-α mRNA in the stromal vascular fraction of this tissue. β-AR-deficient (β-less) mice manifested an increased plasma TNF-α concentration and increased TNF-α mRNA abundance in epiWAT and BAT. TNF-α mRNA abundance was greater in ATMs (CD11b+ cells of the stromal vascular fraction) from epiWAT or BAT of wild-type mice than in corresponding CD11b− cells, and β2-AR mRNA abundance was greater in ATMs than in CD11b− cells of epiWAT. Our results show that the SNS and β2-AR-protein kinase A pathway maintain an anti-inflammatory state in ATMs of lean mice in vivo, and that the brain melanocortin pathway plays a role in maintaining this state in WAT of lean mice via the SNS.</abstract><cop>United States</cop><pub>Endocrine Society</pub><pmid>26132918</pmid><doi>10.1210/EN.2015-1096</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; Journals@Ovid Complete |
| subjects | Abundance Adipose tissue Adipose tissue (brown) Adipose Tissue, Brown - drug effects Adipose Tissue, Brown - innervation Adipose Tissue, Brown - metabolism Adipose Tissue, White - drug effects Adipose Tissue, White - innervation Adipose Tissue, White - metabolism Adrenergic beta-Antagonists - pharmacology Adrenergic receptors Agouti-Related Protein - administration & dosage Animals Body fat CD11b antigen Cell Line Denervation Epididymis - drug effects Epididymis - metabolism Explants Gene expression Gene Expression - drug effects Immunoblotting Inflammation Inflammation Mediators - metabolism Inflammatory response Injections, Intraventricular Intracerebroventricular administration Kinases Lipopolysaccharides Low level Macrophages Macrophages - metabolism Male Melanocortin Mice, Inbred C57BL Mice, Knockout Nerves Peptide Fragments - administration & dosage Propranolol Propranolol - pharmacology Protein kinase A Proteins Receptors (physiology) Receptors, Adrenergic, beta - genetics Receptors, Adrenergic, beta - metabolism Reverse Transcriptase Polymerase Chain Reaction Sympathectomy Sympathetic nerves Sympathetic nervous system Sympathetic Nervous System - metabolism Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-α |
| title | Sympathetic Nerve Activity Maintains an Anti-Inflammatory State in Adipose Tissue in Male Mice by Inhibiting TNF-α Gene Expression in Macrophages |
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