The cAMP Sensor Epac2 Is a Direct Target of Antidiabetic Sulfonylurea Drugs
Epac2, a guanine nucleotide exchange factor for the small guanosine triphosphatase Rap1, is activated by adenosine 3′,5′-monophosphate. Fluorescence resonance energy transfer and binding experiments revealed that sulfonylureas, widely used antidiabetic drugs, interact directly with Epac2. Sulfonylur...
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| Veröffentlicht in: | Science (American Association for the Advancement of Science) 2009-07, Vol.325 (5940), p.607-610 |
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| creator | Zhang, Chang-Liang Katoh, Megumi Shibasaki, Tadao Minami, Kohtaro Sunaga, Yasuhiro Takahashi, Harumi Yokoi, Norihide Iwasaki, Masahiro Miki, Takashi Seino, Susumu |
| description | Epac2, a guanine nucleotide exchange factor for the small guanosine triphosphatase Rap1, is activated by adenosine 3′,5′-monophosphate. Fluorescence resonance energy transfer and binding experiments revealed that sulfonylureas, widely used antidiabetic drugs, interact directly with Epac2. Sulfonylureas activated Rap1 specifically through Epac2. Sulfonylurea-stimulated insulin secretion was reduced both in vitro and in vivo in mice lacking Epac2, and the glucose-lowering effect of the sulfonylurea tolbutamide was decreased in these mice. Epac2 thus contributes to the effect of sulfonylureas to promote insulin secretion. Because Epac2 is also required for the action of incretins, gut hormones crucial for potentiating insulin secretion, it may be a promising target for antidiabetic drug development. |
| doi_str_mv | 10.1126/science.1172256 |
| format | Article |
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Fluorescence resonance energy transfer and binding experiments revealed that sulfonylureas, widely used antidiabetic drugs, interact directly with Epac2. Sulfonylureas activated Rap1 specifically through Epac2. Sulfonylurea-stimulated insulin secretion was reduced both in vitro and in vivo in mice lacking Epac2, and the glucose-lowering effect of the sulfonylurea tolbutamide was decreased in these mice. Epac2 thus contributes to the effect of sulfonylureas to promote insulin secretion. Because Epac2 is also required for the action of incretins, gut hormones crucial for potentiating insulin secretion, it may be a promising target for antidiabetic drug development.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.1172256</identifier><identifier>PMID: 19644119</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Association for the Advancement of Science</publisher><subject>8-Bromo Cyclic Adenosine Monophosphate - pharmacology ; Animals ; Biological and medical sciences ; Biomedical technology ; Blood glucose ; Blood Glucose - analysis ; Carrier Proteins - genetics ; Carrier Proteins - metabolism ; Cell Line ; Cercopithecus aethiops ; COS Cells ; Cyclic AMP - metabolism ; Diabetes ; Fluorescence Resonance Energy Transfer ; Glucose ; Glucose - administration & dosage ; Glyburide - metabolism ; Glyburide - pharmacology ; Guanine Nucleotide Exchange Factors - genetics ; Guanine Nucleotide Exchange Factors - metabolism ; Hormones. Endocrine system ; Hypoglycemic agents ; Hypoglycemic Agents - chemistry ; Hypoglycemic Agents - metabolism ; Hypoglycemic Agents - pharmacology ; Insulin ; Insulin - blood ; Insulin - metabolism ; Insulin Secretion ; Islets of Langerhans - metabolism ; Medical research ; Medical sciences ; Metabolism ; Mice ; Mice, Inbred C57BL ; Pharmacology ; Pharmacology. Drug treatments ; Prescription drugs ; rap1 GTP-Binding Proteins - metabolism ; Rodents ; Sensors ; Sulfonylurea Compounds - chemistry ; Sulfonylurea Compounds - metabolism ; Sulfonylurea Compounds - pharmacology ; Tolbutamide - metabolism ; Tolbutamide - pharmacology ; Vehicles</subject><ispartof>Science (American Association for the Advancement of Science), 2009-07, Vol.325 (5940), p.607-610</ispartof><rights>Copyright 2009 American Association for the Advancement of Science</rights><rights>2009 INIST-CNRS</rights><rights>Copyright © 2009, American Association for the Advancement of Science</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-f727385c62961f0cc43ceeaa0cb60215267ba3108f9deb007e9f853b77bf520f3</citedby><cites>FETCH-LOGICAL-c501t-f727385c62961f0cc43ceeaa0cb60215267ba3108f9deb007e9f853b77bf520f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/20544211$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/20544211$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>315,781,785,804,2885,2886,27929,27930,58022,58255</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21804350$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19644119$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Chang-Liang</creatorcontrib><creatorcontrib>Katoh, Megumi</creatorcontrib><creatorcontrib>Shibasaki, Tadao</creatorcontrib><creatorcontrib>Minami, Kohtaro</creatorcontrib><creatorcontrib>Sunaga, Yasuhiro</creatorcontrib><creatorcontrib>Takahashi, Harumi</creatorcontrib><creatorcontrib>Yokoi, Norihide</creatorcontrib><creatorcontrib>Iwasaki, Masahiro</creatorcontrib><creatorcontrib>Miki, Takashi</creatorcontrib><creatorcontrib>Seino, Susumu</creatorcontrib><title>The cAMP Sensor Epac2 Is a Direct Target of Antidiabetic Sulfonylurea Drugs</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Epac2, a guanine nucleotide exchange factor for the small guanosine triphosphatase Rap1, is activated by adenosine 3′,5′-monophosphate. Fluorescence resonance energy transfer and binding experiments revealed that sulfonylureas, widely used antidiabetic drugs, interact directly with Epac2. Sulfonylureas activated Rap1 specifically through Epac2. Sulfonylurea-stimulated insulin secretion was reduced both in vitro and in vivo in mice lacking Epac2, and the glucose-lowering effect of the sulfonylurea tolbutamide was decreased in these mice. Epac2 thus contributes to the effect of sulfonylureas to promote insulin secretion. Because Epac2 is also required for the action of incretins, gut hormones crucial for potentiating insulin secretion, it may be a promising target for antidiabetic drug development.</description><subject>8-Bromo Cyclic Adenosine Monophosphate - pharmacology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Biomedical technology</subject><subject>Blood glucose</subject><subject>Blood Glucose - analysis</subject><subject>Carrier Proteins - genetics</subject><subject>Carrier Proteins - metabolism</subject><subject>Cell Line</subject><subject>Cercopithecus aethiops</subject><subject>COS Cells</subject><subject>Cyclic AMP - metabolism</subject><subject>Diabetes</subject><subject>Fluorescence Resonance Energy Transfer</subject><subject>Glucose</subject><subject>Glucose - administration & dosage</subject><subject>Glyburide - metabolism</subject><subject>Glyburide - pharmacology</subject><subject>Guanine Nucleotide Exchange Factors - genetics</subject><subject>Guanine Nucleotide Exchange Factors - metabolism</subject><subject>Hormones. Endocrine system</subject><subject>Hypoglycemic agents</subject><subject>Hypoglycemic Agents - chemistry</subject><subject>Hypoglycemic Agents - metabolism</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Insulin</subject><subject>Insulin - blood</subject><subject>Insulin - metabolism</subject><subject>Insulin Secretion</subject><subject>Islets of Langerhans - metabolism</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Pharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Prescription drugs</subject><subject>rap1 GTP-Binding Proteins - metabolism</subject><subject>Rodents</subject><subject>Sensors</subject><subject>Sulfonylurea Compounds - chemistry</subject><subject>Sulfonylurea Compounds - metabolism</subject><subject>Sulfonylurea Compounds - pharmacology</subject><subject>Tolbutamide - metabolism</subject><subject>Tolbutamide - pharmacology</subject><subject>Vehicles</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0cFr2zAUBnBRVpo03bmnDTFob26fJEuyjqHNttCUFZqdjaw8dQ6OnUn2If99NWJa6GUnId5PH-h9hFwyuGGMq9voamwdpovmXKoTMmVgZGY4iE9kCiBUVoCWE3Ie4xYgzYw4IxNmVJ4zZqbkYf0HqZs_PtFnbGMX6GJvHafLSC29rwO6nq5teMGedp7O277e1LbCvnb0eWh81x6aIWCiYXiJF-TU2ybi5_Gckd_fF-u7n9nq14_l3XyVOQmsz7zmWhTSKW4U8-BcLhyiteAqBZxJrnRlBYPCmw1WABqNL6SotK685ODFjFwfc_eh-ztg7MtdHR02jW2xG2KptMyhKNR_oVBcQ1pcgt8-wG03hDZ9ouRMSJOy8oRuj8iFLsaAvtyHemfDoWRQ_mujHNsoxzbSi69j7FDtcPPux_UncDUCG51tfLCtq-Ob46yAXEhI7svRbWPfhfc5yDznjIlXuX-adQ</recordid><startdate>20090731</startdate><enddate>20090731</enddate><creator>Zhang, Chang-Liang</creator><creator>Katoh, Megumi</creator><creator>Shibasaki, Tadao</creator><creator>Minami, Kohtaro</creator><creator>Sunaga, Yasuhiro</creator><creator>Takahashi, Harumi</creator><creator>Yokoi, Norihide</creator><creator>Iwasaki, Masahiro</creator><creator>Miki, Takashi</creator><creator>Seino, Susumu</creator><general>American Association for the Advancement of Science</general><general>The American Association for the Advancement of Science</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>7QF</scope><scope>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QQ</scope><scope>7QR</scope><scope>7SC</scope><scope>7SE</scope><scope>7SN</scope><scope>7SP</scope><scope>7SR</scope><scope>7SS</scope><scope>7T7</scope><scope>7TA</scope><scope>7TB</scope><scope>7TK</scope><scope>7TM</scope><scope>7U5</scope><scope>7U9</scope><scope>8BQ</scope><scope>8FD</scope><scope>C1K</scope><scope>F28</scope><scope>FR3</scope><scope>H8D</scope><scope>H8G</scope><scope>H94</scope><scope>JG9</scope><scope>JQ2</scope><scope>K9.</scope><scope>KR7</scope><scope>L7M</scope><scope>L~C</scope><scope>L~D</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20090731</creationdate><title>The cAMP Sensor Epac2 Is a Direct Target of Antidiabetic Sulfonylurea Drugs</title><author>Zhang, Chang-Liang ; Katoh, Megumi ; Shibasaki, Tadao ; Minami, Kohtaro ; Sunaga, Yasuhiro ; Takahashi, Harumi ; Yokoi, Norihide ; Iwasaki, Masahiro ; Miki, Takashi ; Seino, Susumu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c501t-f727385c62961f0cc43ceeaa0cb60215267ba3108f9deb007e9f853b77bf520f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>8-Bromo Cyclic Adenosine Monophosphate - pharmacology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Biomedical technology</topic><topic>Blood glucose</topic><topic>Blood Glucose - analysis</topic><topic>Carrier Proteins - genetics</topic><topic>Carrier Proteins - metabolism</topic><topic>Cell Line</topic><topic>Cercopithecus aethiops</topic><topic>COS Cells</topic><topic>Cyclic AMP - metabolism</topic><topic>Diabetes</topic><topic>Fluorescence Resonance Energy Transfer</topic><topic>Glucose</topic><topic>Glucose - administration & dosage</topic><topic>Glyburide - metabolism</topic><topic>Glyburide - pharmacology</topic><topic>Guanine Nucleotide Exchange Factors - genetics</topic><topic>Guanine Nucleotide Exchange Factors - metabolism</topic><topic>Hormones. 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Fluorescence resonance energy transfer and binding experiments revealed that sulfonylureas, widely used antidiabetic drugs, interact directly with Epac2. Sulfonylureas activated Rap1 specifically through Epac2. Sulfonylurea-stimulated insulin secretion was reduced both in vitro and in vivo in mice lacking Epac2, and the glucose-lowering effect of the sulfonylurea tolbutamide was decreased in these mice. Epac2 thus contributes to the effect of sulfonylureas to promote insulin secretion. Because Epac2 is also required for the action of incretins, gut hormones crucial for potentiating insulin secretion, it may be a promising target for antidiabetic drug development.</abstract><cop>Washington, DC</cop><pub>American Association for the Advancement of Science</pub><pmid>19644119</pmid><doi>10.1126/science.1172256</doi><tpages>4</tpages></addata></record> |
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| subjects | 8-Bromo Cyclic Adenosine Monophosphate - pharmacology Animals Biological and medical sciences Biomedical technology Blood glucose Blood Glucose - analysis Carrier Proteins - genetics Carrier Proteins - metabolism Cell Line Cercopithecus aethiops COS Cells Cyclic AMP - metabolism Diabetes Fluorescence Resonance Energy Transfer Glucose Glucose - administration & dosage Glyburide - metabolism Glyburide - pharmacology Guanine Nucleotide Exchange Factors - genetics Guanine Nucleotide Exchange Factors - metabolism Hormones. Endocrine system Hypoglycemic agents Hypoglycemic Agents - chemistry Hypoglycemic Agents - metabolism Hypoglycemic Agents - pharmacology Insulin Insulin - blood Insulin - metabolism Insulin Secretion Islets of Langerhans - metabolism Medical research Medical sciences Metabolism Mice Mice, Inbred C57BL Pharmacology Pharmacology. Drug treatments Prescription drugs rap1 GTP-Binding Proteins - metabolism Rodents Sensors Sulfonylurea Compounds - chemistry Sulfonylurea Compounds - metabolism Sulfonylurea Compounds - pharmacology Tolbutamide - metabolism Tolbutamide - pharmacology Vehicles |
| title | The cAMP Sensor Epac2 Is a Direct Target of Antidiabetic Sulfonylurea Drugs |
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