Central Relaxin-3 Administration Causes Hyperphagia in Male Wistar Rats
Relaxin-3 (INSL-7) is a recently discovered member of the insulin superfamily. Relaxin-3 mRNA is expressed in the nucleus incertus of the brainstem, which has projections to the hypothalamus. Relaxin-3 binds with high affinity to the LGR7 receptor and to the previously orphan G protein-coupled recep...
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| Veröffentlicht in: | Endocrinology (Philadelphia) 2005-08, Vol.146 (8), p.3295-3300 |
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| creator | McGowan, B. M. C Stanley, S. A Smith, K. L White, N. E Connolly, M. M Thompson, E. L Gardiner, J. V Murphy, K. G Ghatei, M. A Bloom, S. R |
| description | Relaxin-3 (INSL-7) is a recently discovered member of the insulin superfamily. Relaxin-3 mRNA is expressed in the nucleus incertus of the brainstem, which has projections to the hypothalamus. Relaxin-3 binds with high affinity to the LGR7 receptor and to the previously orphan G protein-coupled receptor GPCR135. GPCR135 mRNA is expressed predominantly in the central nervous system, particularly in the paraventricular nucleus (PVN). The presence of relaxin-3 and these receptors in the PVN led us to investigate the effect of central administration of relaxin-3 on food intake in male Wistar rats. The receptor involved in mediating these effects was also investigated. Intracerebroventricular injections of human relaxin-3 (H3) to satiated rats significantly increased food intake 1 h post administration in the early light phase [0.96 ± 0.16 g (vehicle) vs. 1.81 ± 0.21 g (180 pmol H3), P < 0.05] and the early dark phase [2.95 ± 0.45 g (vehicle) vs. 4.39 ± 0.39 g (180 pmol H3), P < 0.05]. Intra-PVN H3 administration significantly increased 1-h food intake in satiated rats in the early light phase [0.34 ± 0.16 g (vehicle) vs. 1.23 ± 0.30 g (18 pmol H3), P < 0.05] and the early dark phase [4.43 ± 0.32 g (vehicle) vs. 6.57 ± 0.42 g (18 pmol H3), P < 0.05]. Feeding behavior increased after intra-PVN H3. Equimolar doses of human relaxin-2, which binds the LGR7 receptor but not GPCR135, did not increase feeding. Hypothalamic neuropeptide Y, proopiomelanocortin, or agouti-related peptide mRNA expression did not change after acute intracerebroventricular H3. These results suggest a novel role for relaxin-3 in appetite regulation. |
| doi_str_mv | 10.1210/en.2004-1532 |
| format | Article |
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M. C ; Stanley, S. A ; Smith, K. L ; White, N. E ; Connolly, M. M ; Thompson, E. L ; Gardiner, J. V ; Murphy, K. G ; Ghatei, M. A ; Bloom, S. R</creator><creatorcontrib>McGowan, B. M. C ; Stanley, S. A ; Smith, K. L ; White, N. E ; Connolly, M. M ; Thompson, E. L ; Gardiner, J. V ; Murphy, K. G ; Ghatei, M. A ; Bloom, S. R</creatorcontrib><description>Relaxin-3 (INSL-7) is a recently discovered member of the insulin superfamily. Relaxin-3 mRNA is expressed in the nucleus incertus of the brainstem, which has projections to the hypothalamus. Relaxin-3 binds with high affinity to the LGR7 receptor and to the previously orphan G protein-coupled receptor GPCR135. GPCR135 mRNA is expressed predominantly in the central nervous system, particularly in the paraventricular nucleus (PVN). The presence of relaxin-3 and these receptors in the PVN led us to investigate the effect of central administration of relaxin-3 on food intake in male Wistar rats. The receptor involved in mediating these effects was also investigated. Intracerebroventricular injections of human relaxin-3 (H3) to satiated rats significantly increased food intake 1 h post administration in the early light phase [0.96 ± 0.16 g (vehicle) vs. 1.81 ± 0.21 g (180 pmol H3), P < 0.05] and the early dark phase [2.95 ± 0.45 g (vehicle) vs. 4.39 ± 0.39 g (180 pmol H3), P < 0.05]. Intra-PVN H3 administration significantly increased 1-h food intake in satiated rats in the early light phase [0.34 ± 0.16 g (vehicle) vs. 1.23 ± 0.30 g (18 pmol H3), P < 0.05] and the early dark phase [4.43 ± 0.32 g (vehicle) vs. 6.57 ± 0.42 g (18 pmol H3), P < 0.05]. Feeding behavior increased after intra-PVN H3. Equimolar doses of human relaxin-2, which binds the LGR7 receptor but not GPCR135, did not increase feeding. Hypothalamic neuropeptide Y, proopiomelanocortin, or agouti-related peptide mRNA expression did not change after acute intracerebroventricular H3. These results suggest a novel role for relaxin-3 in appetite regulation.</description><identifier>ISSN: 0013-7227</identifier><identifier>EISSN: 1945-7170</identifier><identifier>DOI: 10.1210/en.2004-1532</identifier><identifier>PMID: 15845619</identifier><identifier>CODEN: ENDOAO</identifier><language>eng</language><publisher>Bethesda, MD: Endocrine Society</publisher><subject>Animals ; Biological and medical sciences ; Brain stem ; Central nervous system ; Cerebral Ventricles - drug effects ; Cerebral Ventricles - physiology ; Feeding behavior ; Food ; Food intake ; Fundamental and applied biological sciences. Psychology ; Gene expression ; Gene Expression Regulation - drug effects ; Hyperphagia ; Hyperphagia - chemically induced ; Hypothalamus ; Hypothalamus - physiopathology ; Injections, Intraventricular ; Male ; Males ; Midline Thalamic Nuclei - drug effects ; Midline Thalamic Nuclei - physiology ; Neuropeptide Y ; Neuropeptide Y - genetics ; Paraventricular nucleus ; Pro-Opiomelanocortin - genetics ; Proopiomelanocortin ; Rats ; Rats, Wistar ; Receptors ; Relaxin ; Relaxin - administration & dosage ; Relaxin - pharmacology ; RNA, Messenger - genetics ; Vertebrates: endocrinology</subject><ispartof>Endocrinology (Philadelphia), 2005-08, Vol.146 (8), p.3295-3300</ispartof><rights>Copyright © 2005 by The Endocrine Society 2005</rights><rights>2005 INIST-CNRS</rights><rights>Copyright © 2005 by The Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c558t-bc6e38550015969c2a2b629787d78eb4008204bc9a2a58eb758e3391b97de35e3</citedby><cites>FETCH-LOGICAL-c558t-bc6e38550015969c2a2b629787d78eb4008204bc9a2a58eb758e3391b97de35e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16953061$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15845619$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McGowan, B. M. C</creatorcontrib><creatorcontrib>Stanley, S. A</creatorcontrib><creatorcontrib>Smith, K. L</creatorcontrib><creatorcontrib>White, N. E</creatorcontrib><creatorcontrib>Connolly, M. M</creatorcontrib><creatorcontrib>Thompson, E. L</creatorcontrib><creatorcontrib>Gardiner, J. V</creatorcontrib><creatorcontrib>Murphy, K. G</creatorcontrib><creatorcontrib>Ghatei, M. A</creatorcontrib><creatorcontrib>Bloom, S. R</creatorcontrib><title>Central Relaxin-3 Administration Causes Hyperphagia in Male Wistar Rats</title><title>Endocrinology (Philadelphia)</title><addtitle>Endocrinology</addtitle><description>Relaxin-3 (INSL-7) is a recently discovered member of the insulin superfamily. Relaxin-3 mRNA is expressed in the nucleus incertus of the brainstem, which has projections to the hypothalamus. Relaxin-3 binds with high affinity to the LGR7 receptor and to the previously orphan G protein-coupled receptor GPCR135. GPCR135 mRNA is expressed predominantly in the central nervous system, particularly in the paraventricular nucleus (PVN). The presence of relaxin-3 and these receptors in the PVN led us to investigate the effect of central administration of relaxin-3 on food intake in male Wistar rats. The receptor involved in mediating these effects was also investigated. Intracerebroventricular injections of human relaxin-3 (H3) to satiated rats significantly increased food intake 1 h post administration in the early light phase [0.96 ± 0.16 g (vehicle) vs. 1.81 ± 0.21 g (180 pmol H3), P < 0.05] and the early dark phase [2.95 ± 0.45 g (vehicle) vs. 4.39 ± 0.39 g (180 pmol H3), P < 0.05]. Intra-PVN H3 administration significantly increased 1-h food intake in satiated rats in the early light phase [0.34 ± 0.16 g (vehicle) vs. 1.23 ± 0.30 g (18 pmol H3), P < 0.05] and the early dark phase [4.43 ± 0.32 g (vehicle) vs. 6.57 ± 0.42 g (18 pmol H3), P < 0.05]. Feeding behavior increased after intra-PVN H3. Equimolar doses of human relaxin-2, which binds the LGR7 receptor but not GPCR135, did not increase feeding. Hypothalamic neuropeptide Y, proopiomelanocortin, or agouti-related peptide mRNA expression did not change after acute intracerebroventricular H3. These results suggest a novel role for relaxin-3 in appetite regulation.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain stem</subject><subject>Central nervous system</subject><subject>Cerebral Ventricles - drug effects</subject><subject>Cerebral Ventricles - physiology</subject><subject>Feeding behavior</subject><subject>Food</subject><subject>Food intake</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hyperphagia</subject><subject>Hyperphagia - chemically induced</subject><subject>Hypothalamus</subject><subject>Hypothalamus - physiopathology</subject><subject>Injections, Intraventricular</subject><subject>Male</subject><subject>Males</subject><subject>Midline Thalamic Nuclei - drug effects</subject><subject>Midline Thalamic Nuclei - physiology</subject><subject>Neuropeptide Y</subject><subject>Neuropeptide Y - genetics</subject><subject>Paraventricular nucleus</subject><subject>Pro-Opiomelanocortin - genetics</subject><subject>Proopiomelanocortin</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors</subject><subject>Relaxin</subject><subject>Relaxin - administration & dosage</subject><subject>Relaxin - pharmacology</subject><subject>RNA, Messenger - genetics</subject><subject>Vertebrates: endocrinology</subject><issn>0013-7227</issn><issn>1945-7170</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c1LHDEUAPBQWuqqvfUsA6X10rH5nEyOstQPUARRegxvMm9rZDYzJjNQ_3uz7MBCUbwk5PHj5X0Q8pXRE8YZ_YXhhFMqS6YE_0AWzEhVaqbpR7KglIlSc673yH5Kj_kppRSfyR5TtVQVMwtyvsQwRuiKW-zgnw-lKE7btQ8-5ejo-1AsYUqYiovnAePwAH89FD4U19Bh8ScriMUtjOmQfFpBl_DLfB-Q-7Pfd8uL8urm_HJ5elU6peqxbFyFolYql6JMZRwH3lTc6Fq3usZGUlpzKhtngIPKAZ0PIQxrjG5RKBQH5Mc27xD7pwnTaNc-Oew6CNhPyVY15ZyJ-l3ItMiT4TLDb__Bx36KITdhBRNUaaM4z-rnVrnYpxRxZYfo1xCfLaN2sweLwW72YDd7yPxoTjo1a2x3eB58Bt9nAMlBt4oQnE87VxklaMWyO966fhre-rKcvxRbiaHtXfQBh4gp7bp5tdAX-SWp1w</recordid><startdate>20050801</startdate><enddate>20050801</enddate><creator>McGowan, B. M. C</creator><creator>Stanley, S. A</creator><creator>Smith, K. L</creator><creator>White, N. E</creator><creator>Connolly, M. M</creator><creator>Thompson, E. L</creator><creator>Gardiner, J. V</creator><creator>Murphy, K. G</creator><creator>Ghatei, M. A</creator><creator>Bloom, S. R</creator><general>Endocrine Society</general><general>Oxford University Press</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>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>7TK</scope><scope>7X8</scope></search><sort><creationdate>20050801</creationdate><title>Central Relaxin-3 Administration Causes Hyperphagia in Male Wistar Rats</title><author>McGowan, B. M. C ; Stanley, S. A ; Smith, K. L ; White, N. E ; Connolly, M. M ; Thompson, E. L ; Gardiner, J. V ; Murphy, K. G ; Ghatei, M. A ; Bloom, S. R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c558t-bc6e38550015969c2a2b629787d78eb4008204bc9a2a58eb758e3391b97de35e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain stem</topic><topic>Central nervous system</topic><topic>Cerebral Ventricles - drug effects</topic><topic>Cerebral Ventricles - physiology</topic><topic>Feeding behavior</topic><topic>Food</topic><topic>Food intake</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hyperphagia</topic><topic>Hyperphagia - chemically induced</topic><topic>Hypothalamus</topic><topic>Hypothalamus - physiopathology</topic><topic>Injections, Intraventricular</topic><topic>Male</topic><topic>Males</topic><topic>Midline Thalamic Nuclei - drug effects</topic><topic>Midline Thalamic Nuclei - physiology</topic><topic>Neuropeptide Y</topic><topic>Neuropeptide Y - genetics</topic><topic>Paraventricular nucleus</topic><topic>Pro-Opiomelanocortin - genetics</topic><topic>Proopiomelanocortin</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors</topic><topic>Relaxin</topic><topic>Relaxin - administration & dosage</topic><topic>Relaxin - pharmacology</topic><topic>RNA, Messenger - genetics</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McGowan, B. M. 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M. C</au><au>Stanley, S. A</au><au>Smith, K. L</au><au>White, N. E</au><au>Connolly, M. M</au><au>Thompson, E. L</au><au>Gardiner, J. V</au><au>Murphy, K. G</au><au>Ghatei, M. A</au><au>Bloom, S. R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Central Relaxin-3 Administration Causes Hyperphagia in Male Wistar Rats</atitle><jtitle>Endocrinology (Philadelphia)</jtitle><addtitle>Endocrinology</addtitle><date>2005-08-01</date><risdate>2005</risdate><volume>146</volume><issue>8</issue><spage>3295</spage><epage>3300</epage><pages>3295-3300</pages><issn>0013-7227</issn><eissn>1945-7170</eissn><coden>ENDOAO</coden><abstract>Relaxin-3 (INSL-7) is a recently discovered member of the insulin superfamily. Relaxin-3 mRNA is expressed in the nucleus incertus of the brainstem, which has projections to the hypothalamus. Relaxin-3 binds with high affinity to the LGR7 receptor and to the previously orphan G protein-coupled receptor GPCR135. GPCR135 mRNA is expressed predominantly in the central nervous system, particularly in the paraventricular nucleus (PVN). The presence of relaxin-3 and these receptors in the PVN led us to investigate the effect of central administration of relaxin-3 on food intake in male Wistar rats. The receptor involved in mediating these effects was also investigated. Intracerebroventricular injections of human relaxin-3 (H3) to satiated rats significantly increased food intake 1 h post administration in the early light phase [0.96 ± 0.16 g (vehicle) vs. 1.81 ± 0.21 g (180 pmol H3), P < 0.05] and the early dark phase [2.95 ± 0.45 g (vehicle) vs. 4.39 ± 0.39 g (180 pmol H3), P < 0.05]. Intra-PVN H3 administration significantly increased 1-h food intake in satiated rats in the early light phase [0.34 ± 0.16 g (vehicle) vs. 1.23 ± 0.30 g (18 pmol H3), P < 0.05] and the early dark phase [4.43 ± 0.32 g (vehicle) vs. 6.57 ± 0.42 g (18 pmol H3), P < 0.05]. Feeding behavior increased after intra-PVN H3. Equimolar doses of human relaxin-2, which binds the LGR7 receptor but not GPCR135, did not increase feeding. Hypothalamic neuropeptide Y, proopiomelanocortin, or agouti-related peptide mRNA expression did not change after acute intracerebroventricular H3. These results suggest a novel role for relaxin-3 in appetite regulation.</abstract><cop>Bethesda, MD</cop><pub>Endocrine Society</pub><pmid>15845619</pmid><doi>10.1210/en.2004-1532</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Biological and medical sciences Brain stem Central nervous system Cerebral Ventricles - drug effects Cerebral Ventricles - physiology Feeding behavior Food Food intake Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation - drug effects Hyperphagia Hyperphagia - chemically induced Hypothalamus Hypothalamus - physiopathology Injections, Intraventricular Male Males Midline Thalamic Nuclei - drug effects Midline Thalamic Nuclei - physiology Neuropeptide Y Neuropeptide Y - genetics Paraventricular nucleus Pro-Opiomelanocortin - genetics Proopiomelanocortin Rats Rats, Wistar Receptors Relaxin Relaxin - administration & dosage Relaxin - pharmacology RNA, Messenger - genetics Vertebrates: endocrinology |
| title | Central Relaxin-3 Administration Causes Hyperphagia in Male Wistar Rats |
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