Possible role of the adrenergic mechanism in gastric inhibitory polypeptide-and glucagon-like peptide-1 (7–36) amide-induced insulin release in the rat
Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1(7–36) amide (GLP-1) are thought to be the most probable candidates for incretin. However, the precise mechanism of incretin effect is unclear. In the present study, to elucidate the possible role of the autonomic nervous system in incr...
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| Veröffentlicht in: | Metabolism, clinical and experimental clinical and experimental, 1993-02, Vol.42 (2), p.209-213 |
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| container_title | Metabolism, clinical and experimental |
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| creator | Ikeda, Tadasu Ochi, Hiroshi Ohtani, Izumi Fujiyama, Katsumi Hoshino, Tazue Tanaka, Yasushi Takeuchi, Tatsuo Mashiba, Hiroto |
| description | Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1(7–36) amide (GLP-1) are thought to be the most probable candidates for incretin. However, the precise mechanism of incretin effect is unclear. In the present study, to elucidate the possible role of the autonomic nervous system in incretin effect, the effects of atropine, propranolol, metoprolol, and phentolamine on GIP- or GLP-1-induced insulin release were investigated in the rat. The GIP-induced (2 or 20μg) insulin release was partly inhibited by propranolol pretreatment (0.5 mg/kg subcutaneously [SC]), and GLP-1-induced (2 or 20 μg) insulin release was partly inhibited by propranolol or metoprolol (35 mg/kg SC). These results suggest that a β-adrenergic mechanism may be involved in the incretin effect, probably through a modulating effect on GIP- or GLP-1-induced insulin secretion. |
| doi_str_mv | 10.1016/0026-0495(93)90037-O |
| format | Article |
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However, the precise mechanism of incretin effect is unclear. In the present study, to elucidate the possible role of the autonomic nervous system in incretin effect, the effects of atropine, propranolol, metoprolol, and phentolamine on GIP- or GLP-1-induced insulin release were investigated in the rat. The GIP-induced (2 or 20μg) insulin release was partly inhibited by propranolol pretreatment (0.5 mg/kg subcutaneously [SC]), and GLP-1-induced (2 or 20 μg) insulin release was partly inhibited by propranolol or metoprolol (35 mg/kg SC). These results suggest that a β-adrenergic mechanism may be involved in the incretin effect, probably through a modulating effect on GIP- or GLP-1-induced insulin secretion.</description><identifier>ISSN: 0026-0495</identifier><identifier>EISSN: 1532-8600</identifier><identifier>DOI: 10.1016/0026-0495(93)90037-O</identifier><identifier>PMID: 8386288</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Animals ; Biological and medical sciences ; Blood Glucose - analysis ; Endocrine pancreas ; Fundamental and applied biological sciences. Psychology ; Gastric Inhibitory Polypeptide - pharmacology ; Glucagon - pharmacology ; Glucagon-Like Peptide 1 ; Glucagon-Like Peptides ; Hormones. Régulation ; Insulin - blood ; Insulin - metabolism ; Insulin Secretion ; Male ; Peptide Fragments - pharmacology ; Propranolol - pharmacology ; Rats ; Rats, Wistar ; Receptors, Adrenergic, beta - physiology ; Vertebrates: endocrinology</subject><ispartof>Metabolism, clinical and experimental, 1993-02, Vol.42 (2), p.209-213</ispartof><rights>1993</rights><rights>1993 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c301t-71f01d3217a2019668bcc77c567625654d27f8fd2292e318bd4deae0fce6cc083</citedby><cites>FETCH-LOGICAL-c301t-71f01d3217a2019668bcc77c567625654d27f8fd2292e318bd4deae0fce6cc083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/0026-0495(93)90037-O$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=4682737$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8386288$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ikeda, Tadasu</creatorcontrib><creatorcontrib>Ochi, Hiroshi</creatorcontrib><creatorcontrib>Ohtani, Izumi</creatorcontrib><creatorcontrib>Fujiyama, Katsumi</creatorcontrib><creatorcontrib>Hoshino, Tazue</creatorcontrib><creatorcontrib>Tanaka, Yasushi</creatorcontrib><creatorcontrib>Takeuchi, Tatsuo</creatorcontrib><creatorcontrib>Mashiba, Hiroto</creatorcontrib><title>Possible role of the adrenergic mechanism in gastric inhibitory polypeptide-and glucagon-like peptide-1 (7–36) amide-induced insulin release in the rat</title><title>Metabolism, clinical and experimental</title><addtitle>Metabolism</addtitle><description>Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1(7–36) amide (GLP-1) are thought to be the most probable candidates for incretin. However, the precise mechanism of incretin effect is unclear. In the present study, to elucidate the possible role of the autonomic nervous system in incretin effect, the effects of atropine, propranolol, metoprolol, and phentolamine on GIP- or GLP-1-induced insulin release were investigated in the rat. The GIP-induced (2 or 20μg) insulin release was partly inhibited by propranolol pretreatment (0.5 mg/kg subcutaneously [SC]), and GLP-1-induced (2 or 20 μg) insulin release was partly inhibited by propranolol or metoprolol (35 mg/kg SC). These results suggest that a β-adrenergic mechanism may be involved in the incretin effect, probably through a modulating effect on GIP- or GLP-1-induced insulin secretion.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Glucose - analysis</subject><subject>Endocrine pancreas</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gastric Inhibitory Polypeptide - pharmacology</subject><subject>Glucagon - pharmacology</subject><subject>Glucagon-Like Peptide 1</subject><subject>Glucagon-Like Peptides</subject><subject>Hormones. Régulation</subject><subject>Insulin - blood</subject><subject>Insulin - metabolism</subject><subject>Insulin Secretion</subject><subject>Male</subject><subject>Peptide Fragments - pharmacology</subject><subject>Propranolol - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Adrenergic, beta - physiology</subject><subject>Vertebrates: endocrinology</subject><issn>0026-0495</issn><issn>1532-8600</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU2O1DAQhS0EGpqBG4DkBUIzi4B_EtvZjIRG_EkjNQtYW45d6TY4TrATpN5xB1Zcj5Pg0E0v2dhSva9elV4h9JSSl5RQ8YoQJipSt81Vy69bQristvfQhjacVUoQch9tzshD9CjnL4QQKZW4QBeKK8GU2qBfH8ecfRcAp7E8Y4_nPWDjEkRIO2_xAHZvos8D9hHvTJ5TKfq4952fx3TA0xgOE0yzd1CZ6PAuLNbsxlgF_xXwP4XiK_n7x08urrEZ1oKPbrHgilNeQnFOEMBkWIesCyQzP0YPehMyPDn9l-jz2zefbt9Xd9t3H25f31WWEzpXkvaEOs6oNIzQVgjVWSulbYQUrBFN7ZjsVe8YaxlwqjpXOzBAegvCWqL4JXpx9J3S-G2BPOvBZwshmAjjkrVshGJUtAWsj6BNJbMEvZ6SH0w6aEr0ehG9xq3XuHXL9d-L6G1pe3byX7oB3LnpdIKiPz_pJlsT-mSi9fmM1WW65LJgN0cMShbfPSSdrYdYMvQJ7Kzd6P-_xx89MKnb</recordid><startdate>199302</startdate><enddate>199302</enddate><creator>Ikeda, Tadasu</creator><creator>Ochi, Hiroshi</creator><creator>Ohtani, Izumi</creator><creator>Fujiyama, Katsumi</creator><creator>Hoshino, Tazue</creator><creator>Tanaka, Yasushi</creator><creator>Takeuchi, Tatsuo</creator><creator>Mashiba, Hiroto</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>199302</creationdate><title>Possible role of the adrenergic mechanism in gastric inhibitory polypeptide-and glucagon-like peptide-1 (7–36) amide-induced insulin release in the rat</title><author>Ikeda, Tadasu ; Ochi, Hiroshi ; Ohtani, Izumi ; Fujiyama, Katsumi ; Hoshino, Tazue ; Tanaka, Yasushi ; Takeuchi, Tatsuo ; Mashiba, Hiroto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c301t-71f01d3217a2019668bcc77c567625654d27f8fd2292e318bd4deae0fce6cc083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Glucose - analysis</topic><topic>Endocrine pancreas</topic><topic>Fundamental and applied biological sciences. 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Régulation</topic><topic>Insulin - blood</topic><topic>Insulin - metabolism</topic><topic>Insulin Secretion</topic><topic>Male</topic><topic>Peptide Fragments - pharmacology</topic><topic>Propranolol - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Adrenergic, beta - physiology</topic><topic>Vertebrates: endocrinology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ikeda, Tadasu</creatorcontrib><creatorcontrib>Ochi, Hiroshi</creatorcontrib><creatorcontrib>Ohtani, Izumi</creatorcontrib><creatorcontrib>Fujiyama, Katsumi</creatorcontrib><creatorcontrib>Hoshino, Tazue</creatorcontrib><creatorcontrib>Tanaka, Yasushi</creatorcontrib><creatorcontrib>Takeuchi, Tatsuo</creatorcontrib><creatorcontrib>Mashiba, Hiroto</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>Ikeda, Tadasu</au><au>Ochi, Hiroshi</au><au>Ohtani, Izumi</au><au>Fujiyama, Katsumi</au><au>Hoshino, Tazue</au><au>Tanaka, Yasushi</au><au>Takeuchi, Tatsuo</au><au>Mashiba, Hiroto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Possible role of the adrenergic mechanism in gastric inhibitory polypeptide-and glucagon-like peptide-1 (7–36) amide-induced insulin release in the rat</atitle><jtitle>Metabolism, clinical and experimental</jtitle><addtitle>Metabolism</addtitle><date>1993-02</date><risdate>1993</risdate><volume>42</volume><issue>2</issue><spage>209</spage><epage>213</epage><pages>209-213</pages><issn>0026-0495</issn><eissn>1532-8600</eissn><abstract>Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1(7–36) amide (GLP-1) are thought to be the most probable candidates for incretin. However, the precise mechanism of incretin effect is unclear. In the present study, to elucidate the possible role of the autonomic nervous system in incretin effect, the effects of atropine, propranolol, metoprolol, and phentolamine on GIP- or GLP-1-induced insulin release were investigated in the rat. The GIP-induced (2 or 20μg) insulin release was partly inhibited by propranolol pretreatment (0.5 mg/kg subcutaneously [SC]), and GLP-1-induced (2 or 20 μg) insulin release was partly inhibited by propranolol or metoprolol (35 mg/kg SC). These results suggest that a β-adrenergic mechanism may be involved in the incretin effect, probably through a modulating effect on GIP- or GLP-1-induced insulin secretion.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>8386288</pmid><doi>10.1016/0026-0495(93)90037-O</doi><tpages>5</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Blood Glucose - analysis Endocrine pancreas Fundamental and applied biological sciences. Psychology Gastric Inhibitory Polypeptide - pharmacology Glucagon - pharmacology Glucagon-Like Peptide 1 Glucagon-Like Peptides Hormones. Régulation Insulin - blood Insulin - metabolism Insulin Secretion Male Peptide Fragments - pharmacology Propranolol - pharmacology Rats Rats, Wistar Receptors, Adrenergic, beta - physiology Vertebrates: endocrinology |
| title | Possible role of the adrenergic mechanism in gastric inhibitory polypeptide-and glucagon-like peptide-1 (7–36) amide-induced insulin release in the rat |
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