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Anti-diabetic actions of glucagon-like peptide-1 on pancreatic beta-cells

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dc.contributor.authorLee, Young-Sun-
dc.contributor.authorJun, Hee-Sook-
dc.date.available2020-02-28T18:44:11Z-
dc.date.created2020-02-06-
dc.date.issued2014-01-
dc.identifier.issn0026-0495-
dc.identifier.urihttps://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12952-
dc.description.abstractGlucagon-like peptide-1 (GLP-1), an incretin hormone, is released from intestinal L-cells in response to nutrients. GLP-1 lowers blood glucose levels by stimulating insulin secretion from pancreatic beta-cells in a glucose-dependent manner. In addition, GLP-1 slows gastric emptying, suppresses appetite, reduces plasma glucagon, and stimulates glucose disposal, which are beneficial for glucose homeostasis. Therefore, incretin-based therapies such as GLP-1 receptor agonists and inhibitors of dipeptidyl peptidase IV, an enzyme which inactivates GLP-1, have been developed for treatment of diabetes. This review outlines our knowledge of the actions of GLP-1 on insulin secretion and biosynthesis, beta-cell proliferation and regeneration, and protection against beta-cell damage, as well as the involvement of recently discovered signaling pathways of GLP-1 action, mainly focusing on pancreatic beta-cells. (C) 2014 Elsevier Inc. All rights reserved.-
dc.language영어-
dc.language.isoen-
dc.publisherW B SAUNDERS CO-ELSEVIER INC-
dc.relation.isPartOfMETABOLISM-CLINICAL AND EXPERIMENTAL-
dc.subjectSTIMULATED INSULIN-SECRETION-
dc.subjectIMPROVED GLUCOSE-HOMEOSTASIS-
dc.subjectGENE PROMOTER ACTIVITY-
dc.subjectPROTEIN-KINASE-
dc.subjectALPHA-CELLS-
dc.subjectGLP-1 RECEPTOR-
dc.subjectDIABETIC-RATS-
dc.subjectNOD MICE-
dc.subjectTRANSCRIPTION FACTORS-
dc.subjectCOMBINATION THERAPY-
dc.titleAnti-diabetic actions of glucagon-like peptide-1 on pancreatic beta-cells-
dc.typeArticle-
dc.type.rimsART-
dc.description.journalClass1-
dc.identifier.wosid000328799400003-
dc.identifier.doi10.1016/j.metabol.2013.09.010-
dc.identifier.bibliographicCitationMETABOLISM-CLINICAL AND EXPERIMENTAL, v.63, no.1, pp.9 - 19-
dc.identifier.scopusid2-s2.0-84890118673-
dc.citation.endPage19-
dc.citation.startPage9-
dc.citation.titleMETABOLISM-CLINICAL AND EXPERIMENTAL-
dc.citation.volume63-
dc.citation.number1-
dc.contributor.affiliatedAuthorLee, Young-Sun-
dc.contributor.affiliatedAuthorJun, Hee-Sook-
dc.type.docTypeReview-
dc.subject.keywordAuthorPancreatic islet-
dc.subject.keywordAuthorIncretin hormone-
dc.subject.keywordAuthorType 2 diabetes-
dc.subject.keywordAuthorProliferation-
dc.subject.keywordAuthorAnti-apoptosis-
dc.subject.keywordPlusSTIMULATED INSULIN-SECRETION-
dc.subject.keywordPlusIMPROVED GLUCOSE-HOMEOSTASIS-
dc.subject.keywordPlusGENE PROMOTER ACTIVITY-
dc.subject.keywordPlusPROTEIN-KINASE-
dc.subject.keywordPlusALPHA-CELLS-
dc.subject.keywordPlusGLP-1 RECEPTOR-
dc.subject.keywordPlusDIABETIC-RATS-
dc.subject.keywordPlusNOD MICE-
dc.subject.keywordPlusTRANSCRIPTION FACTORS-
dc.subject.keywordPlusCOMBINATION THERAPY-
dc.relation.journalResearchAreaEndocrinology & Metabolism-
dc.relation.journalWebOfScienceCategoryEndocrinology & Metabolism-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
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