Glucagon-like peptide (GLP-1) is involved in the central modulation of fecal output in rats
In addition to its insulinotropic action, exogenously administered glucagon-like peptide (GLP-1) inhibits gastropancreatic motility and secretion via central pathways. The aims of the present study were to evaluate the effects of exogenous GLP-1-(7-36) amide on fecal output and to investigate the ro...
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| Veröffentlicht in: | American journal of physiology: Gastrointestinal and liver physiology 2000-06, Vol.278 (6), p.G924-G929 |
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| container_title | American journal of physiology: Gastrointestinal and liver physiology |
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| creator | Gülpinar, M A Bozkurt, A Coşkun, T Ulusoy, N B Yegen, B C |
| description | In addition to its insulinotropic action, exogenously administered glucagon-like peptide (GLP-1) inhibits gastropancreatic motility and secretion via central pathways. The aims of the present study were to evaluate the effects of exogenous GLP-1-(7-36) amide on fecal output and to investigate the role of endogenous GLP-1 on stress-induced colonic activity. With the use of a stereotaxic instrument, adult male Sprague-Dawley rats weighing 200-250 g were fitted with stainless steel cerebroventricular guide cannulas under ketamine anesthesia. A group of rats were placed in Bollman-type cages to induce restraint stress. Fecal output monitored for 2 h was increased significantly by intracerebroventricular GLP-1 to 500, 1, 000, and 3,000 pmol/rat (P < 0.05-0.01), whereas intraperitoneal GLP-1 had no effect. Intracerebroventricular administration of the GLP-1 receptor antagonist exendin-(9-39) (10 nmol/rat) reversed the increases induced by GLP-1 (500 pmol/rat; P |
| doi_str_mv | 10.1152/ajpgi.2000.278.6.g924 |
| format | Article |
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The aims of the present study were to evaluate the effects of exogenous GLP-1-(7-36) amide on fecal output and to investigate the role of endogenous GLP-1 on stress-induced colonic activity. With the use of a stereotaxic instrument, adult male Sprague-Dawley rats weighing 200-250 g were fitted with stainless steel cerebroventricular guide cannulas under ketamine anesthesia. A group of rats were placed in Bollman-type cages to induce restraint stress. Fecal output monitored for 2 h was increased significantly by intracerebroventricular GLP-1 to 500, 1, 000, and 3,000 pmol/rat (P < 0.05-0.01), whereas intraperitoneal GLP-1 had no effect. Intracerebroventricular administration of the GLP-1 receptor antagonist exendin-(9-39) (10 nmol/rat) reversed the increases induced by GLP-1 (500 pmol/rat; P<0.01). Similar results were also observed with the injection of corticotropin-releasing factor receptor antagonist astressin (10 microg/rat icv). The significant increase in fecal pellet output induced by restraint stress was also decreased by both intracerebroventricular exendin (10 nmol/rat) and astressin (10 microg/rat; P<0.01-0.001). These results suggest that GLP-1 participates in the central, but not peripheral, regulation of colonic motility via its own receptor and that GLP-1 is likely to be a candidate brain-gut peptide that acts as a physiological modulator of stress-induced colonic motility.</description><identifier>ISSN: 0193-1857</identifier><identifier>EISSN: 1522-1547</identifier><identifier>DOI: 10.1152/ajpgi.2000.278.6.g924</identifier><identifier>PMID: 10859222</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Brain - physiology ; Corticotropin-Releasing Hormone - pharmacology ; Defecation - drug effects ; Defecation - physiology ; Glucagon - pharmacology ; Glucagon - physiology ; Glucagon-Like Peptide 1 ; Glucagon-Like Peptide-1 Receptor ; Injections, Intraperitoneal ; Injections, Intraventricular ; Male ; Peptide Fragments - pharmacology ; Peptide Fragments - physiology ; Protein Precursors - pharmacology ; Protein Precursors - physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Glucagon - antagonists & inhibitors ; Restraint, Physical ; Space life sciences ; Stress, Physiological - physiopathology</subject><ispartof>American journal of physiology: Gastrointestinal and liver physiology, 2000-06, Vol.278 (6), p.G924-G929</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c371t-8b85aadb273e90ca546e49c252005573d424db3f8804a6fe8b576979fccd53cf3</citedby><cites>FETCH-LOGICAL-c371t-8b85aadb273e90ca546e49c252005573d424db3f8804a6fe8b576979fccd53cf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10859222$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gülpinar, M A</creatorcontrib><creatorcontrib>Bozkurt, A</creatorcontrib><creatorcontrib>Coşkun, T</creatorcontrib><creatorcontrib>Ulusoy, N B</creatorcontrib><creatorcontrib>Yegen, B C</creatorcontrib><title>Glucagon-like peptide (GLP-1) is involved in the central modulation of fecal output in rats</title><title>American journal of physiology: Gastrointestinal and liver physiology</title><addtitle>Am J Physiol Gastrointest Liver Physiol</addtitle><description>In addition to its insulinotropic action, exogenously administered glucagon-like peptide (GLP-1) inhibits gastropancreatic motility and secretion via central pathways. The aims of the present study were to evaluate the effects of exogenous GLP-1-(7-36) amide on fecal output and to investigate the role of endogenous GLP-1 on stress-induced colonic activity. With the use of a stereotaxic instrument, adult male Sprague-Dawley rats weighing 200-250 g were fitted with stainless steel cerebroventricular guide cannulas under ketamine anesthesia. A group of rats were placed in Bollman-type cages to induce restraint stress. Fecal output monitored for 2 h was increased significantly by intracerebroventricular GLP-1 to 500, 1, 000, and 3,000 pmol/rat (P < 0.05-0.01), whereas intraperitoneal GLP-1 had no effect. Intracerebroventricular administration of the GLP-1 receptor antagonist exendin-(9-39) (10 nmol/rat) reversed the increases induced by GLP-1 (500 pmol/rat; P<0.01). Similar results were also observed with the injection of corticotropin-releasing factor receptor antagonist astressin (10 microg/rat icv). The significant increase in fecal pellet output induced by restraint stress was also decreased by both intracerebroventricular exendin (10 nmol/rat) and astressin (10 microg/rat; P<0.01-0.001). These results suggest that GLP-1 participates in the central, but not peripheral, regulation of colonic motility via its own receptor and that GLP-1 is likely to be a candidate brain-gut peptide that acts as a physiological modulator of stress-induced colonic motility.</description><subject>Animals</subject><subject>Brain - physiology</subject><subject>Corticotropin-Releasing Hormone - pharmacology</subject><subject>Defecation - drug effects</subject><subject>Defecation - physiology</subject><subject>Glucagon - pharmacology</subject><subject>Glucagon - physiology</subject><subject>Glucagon-Like Peptide 1</subject><subject>Glucagon-Like Peptide-1 Receptor</subject><subject>Injections, Intraperitoneal</subject><subject>Injections, Intraventricular</subject><subject>Male</subject><subject>Peptide Fragments - pharmacology</subject><subject>Peptide Fragments - physiology</subject><subject>Protein Precursors - pharmacology</subject><subject>Protein Precursors - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Glucagon - antagonists & inhibitors</subject><subject>Restraint, Physical</subject><subject>Space life sciences</subject><subject>Stress, Physiological - physiopathology</subject><issn>0193-1857</issn><issn>1522-1547</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkD1PwzAQQC0EoqXwE0CeEAwJ_ojjeEQVBKRKMMDEYDmOU1ySOMROJf49Lu3AdKe7d3e6B8AlRinGjNypzbC2KUEIpYQXaZ6uBcmOwDz2SIJZxo_BHGFBE1wwPgNn3m8iywjGp2CGUcEEIWQOPsp20mrt-qS1XwYOZgi2NvCmXL0m-BZaD22_de3W1DGB4dNAbfowqhZ2rp5aFazroWtgY3SsuSkMU9iRowr-HJw0qvXm4hAX4P3x4W35lKxeyufl_SrRlOOQFFXBlKorwqkRSCuW5SYTmrD4HGOc1hnJ6oo2RYEylTemqBjPBReN1jWjuqELcL3fO4zuezI-yM56bdpW9cZNXnKMBRMojyDbg3p03o-mkcNoOzX-SIzkzqr8syp3VmW0KnNZRqtx7upwYKo6U_-b2mukvy8CdDk</recordid><startdate>20000601</startdate><enddate>20000601</enddate><creator>Gülpinar, M A</creator><creator>Bozkurt, A</creator><creator>Coşkun, T</creator><creator>Ulusoy, N B</creator><creator>Yegen, B C</creator><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>20000601</creationdate><title>Glucagon-like peptide (GLP-1) is involved in the central modulation of fecal output in rats</title><author>Gülpinar, M A ; Bozkurt, A ; Coşkun, T ; Ulusoy, N B ; Yegen, B C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c371t-8b85aadb273e90ca546e49c252005573d424db3f8804a6fe8b576979fccd53cf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Animals</topic><topic>Brain - physiology</topic><topic>Corticotropin-Releasing Hormone - pharmacology</topic><topic>Defecation - drug effects</topic><topic>Defecation - physiology</topic><topic>Glucagon - pharmacology</topic><topic>Glucagon - physiology</topic><topic>Glucagon-Like Peptide 1</topic><topic>Glucagon-Like Peptide-1 Receptor</topic><topic>Injections, Intraperitoneal</topic><topic>Injections, Intraventricular</topic><topic>Male</topic><topic>Peptide Fragments - pharmacology</topic><topic>Peptide Fragments - physiology</topic><topic>Protein Precursors - pharmacology</topic><topic>Protein Precursors - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Glucagon - antagonists & inhibitors</topic><topic>Restraint, Physical</topic><topic>Space life sciences</topic><topic>Stress, Physiological - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gülpinar, M A</creatorcontrib><creatorcontrib>Bozkurt, A</creatorcontrib><creatorcontrib>Coşkun, T</creatorcontrib><creatorcontrib>Ulusoy, N B</creatorcontrib><creatorcontrib>Yegen, B C</creatorcontrib><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>American journal of physiology: Gastrointestinal and liver physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gülpinar, M A</au><au>Bozkurt, A</au><au>Coşkun, T</au><au>Ulusoy, N B</au><au>Yegen, B C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Glucagon-like peptide (GLP-1) is involved in the central modulation of fecal output in rats</atitle><jtitle>American journal of physiology: Gastrointestinal and liver physiology</jtitle><addtitle>Am J Physiol Gastrointest Liver Physiol</addtitle><date>2000-06-01</date><risdate>2000</risdate><volume>278</volume><issue>6</issue><spage>G924</spage><epage>G929</epage><pages>G924-G929</pages><issn>0193-1857</issn><eissn>1522-1547</eissn><abstract>In addition to its insulinotropic action, exogenously administered glucagon-like peptide (GLP-1) inhibits gastropancreatic motility and secretion via central pathways. The aims of the present study were to evaluate the effects of exogenous GLP-1-(7-36) amide on fecal output and to investigate the role of endogenous GLP-1 on stress-induced colonic activity. With the use of a stereotaxic instrument, adult male Sprague-Dawley rats weighing 200-250 g were fitted with stainless steel cerebroventricular guide cannulas under ketamine anesthesia. A group of rats were placed in Bollman-type cages to induce restraint stress. Fecal output monitored for 2 h was increased significantly by intracerebroventricular GLP-1 to 500, 1, 000, and 3,000 pmol/rat (P < 0.05-0.01), whereas intraperitoneal GLP-1 had no effect. Intracerebroventricular administration of the GLP-1 receptor antagonist exendin-(9-39) (10 nmol/rat) reversed the increases induced by GLP-1 (500 pmol/rat; P<0.01). Similar results were also observed with the injection of corticotropin-releasing factor receptor antagonist astressin (10 microg/rat icv). The significant increase in fecal pellet output induced by restraint stress was also decreased by both intracerebroventricular exendin (10 nmol/rat) and astressin (10 microg/rat; P<0.01-0.001). These results suggest that GLP-1 participates in the central, but not peripheral, regulation of colonic motility via its own receptor and that GLP-1 is likely to be a candidate brain-gut peptide that acts as a physiological modulator of stress-induced colonic motility.</abstract><cop>United States</cop><pmid>10859222</pmid><doi>10.1152/ajpgi.2000.278.6.g924</doi></addata></record> |
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| source | MEDLINE; American Physiological Society; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Animals Brain - physiology Corticotropin-Releasing Hormone - pharmacology Defecation - drug effects Defecation - physiology Glucagon - pharmacology Glucagon - physiology Glucagon-Like Peptide 1 Glucagon-Like Peptide-1 Receptor Injections, Intraperitoneal Injections, Intraventricular Male Peptide Fragments - pharmacology Peptide Fragments - physiology Protein Precursors - pharmacology Protein Precursors - physiology Rats Rats, Sprague-Dawley Receptors, Glucagon - antagonists & inhibitors Restraint, Physical Space life sciences Stress, Physiological - physiopathology |
| title | Glucagon-like peptide (GLP-1) is involved in the central modulation of fecal output in rats |
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