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Blockade of cannabinoid 1 receptor improves glucose responsiveness in pancreatic beta cells

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dc.contributor.authorHanho Shin-
dc.contributor.authorJi Hye Han-
dc.contributor.authorJuhwan Yoon-
dc.contributor.authorHyo Jung Sim-
dc.contributor.authorTae Joo Park-
dc.contributor.authorSiyoung Yang-
dc.contributor.authorEun Kyung Lee-
dc.contributor.authorRohit N. Kulkarni-
dc.contributor.authorJosephine M. Egan-
dc.contributor.authorWook Kim-
dc.date.available2019-01-03T05:34:26Z-
dc.date.created2018-05-16-
dc.date.issued2018-02-
dc.identifier.issn1582-4934-
dc.identifier.urihttps://pr.ibs.re.kr/handle/8788114/5300-
dc.description.abstractCannabinoid 1 receptors (CB1Rs) are expressed in peripheral tissues, including islets of Langerhans, where their function(s) is under scrutiny. Using mouse beta-cell lines, human islets and CB1R-null (CB1R(-/-)) mice, we have now investigated the role of CB1Rs in modulating beta-cell function and glucose responsiveness. Synthetic CB1R agonists diminished GLP-1-mediated cAMP accumulation and insulin secretion as well as glucose-stimulated insulin secretion in mouse beta-cell lines and human islets. In addition, silencing CB1R in mouse cells resulted in an increased expression of pro-insulin, glucokinase (GCK) and glucose transporter 2 (GLUT2), but this increase was lost in cells lacking insulin receptor. Furthermore, CB1R(-/-) mice had increased pro-insulin, GCK and GLUT2 expression in cells. Our results suggest that CB1R signalling in pancreatic islets may be harnessed to improve beta-cell glucose responsiveness and preserve their function. Thus, our findings further support that blocking peripheral CB1Rs would be beneficial to beta-cell function in type 2 diabetes. © 2018 The Authors.-
dc.description.uri1-
dc.language영어-
dc.publisherWILEY-
dc.subjectbeta-cell function-
dc.subjectcannabinoid 1 receptor-
dc.subjectglucokinase-
dc.subjectglucose transporter 2-
dc.subjectinsulin secretion-
dc.titleBlockade of cannabinoid 1 receptor improves glucose responsiveness in pancreatic beta cells-
dc.typeArticle-
dc.type.rimsART-
dc.identifier.wosid000428418200028-
dc.identifier.scopusid2-s2.0-85041912512-
dc.identifier.rimsid63259-
dc.contributor.affiliatedAuthorHyo Jung Sim-
dc.contributor.affiliatedAuthorTae Joo Park-
dc.identifier.doi10.1111/jcmm.13523-
dc.identifier.bibliographicCitationJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, v.22, no.4, pp.2337 - 2345-
dc.citation.titleJOURNAL OF CELLULAR AND MOLECULAR MEDICINE-
dc.citation.volume22-
dc.citation.number4-
dc.citation.startPage2337-
dc.citation.endPage2345-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.subject.keywordPlusGLUCAGON-LIKE PEPTIDE-1-
dc.subject.keywordPlusINSULIN-SECRETION-
dc.subject.keywordPlusCB1 RECEPTOR-
dc.subject.keywordPlusADIPOSE-TISSUE-
dc.subject.keywordPlusCONCURRENT STIMULATION-
dc.subject.keywordPlusENDOCANNABINOID SYSTEM-
dc.subject.keywordPlusSIGNAL-TRANSDUCTION-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusMICE-
dc.subject.keywordPlusDIET-
dc.subject.keywordAuthorbeta-cell function-
dc.subject.keywordAuthorcannabinoid 1 receptor-
dc.subject.keywordAuthorglucokinase-
dc.subject.keywordAuthorglucose transporter 2-
dc.subject.keywordAuthorinsulin secretion-
Appears in Collections:
Center for Genomic Integrity(유전체 항상성 연구단) > 1. Journal Papers (저널논문)
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2018_J Cell. Mol. Med._Blockade of cannabinoid 1 receptor improves glucoseresponsiveness in pancreatic beta cells.pdfDownload

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