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DC Field | Value | Language |
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dc.citation.endPage | 10679 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | 10668 | - |
dc.citation.title | FASEB JOURNAL | - |
dc.citation.volume | 33 | - |
dc.contributor.author | Hwang, Hyeon-Jeong | - |
dc.contributor.author | Yang, Yong Ryoul | - |
dc.contributor.author | Kim, Hye Yun | - |
dc.contributor.author | Choi, Yoonji | - |
dc.contributor.author | Park, Kyoung-Su | - |
dc.contributor.author | Lee, Ho | - |
dc.contributor.author | Ma, Ji Su | - |
dc.contributor.author | Yamamoto, Masahiro | - |
dc.contributor.author | Kim, Jaeyoon | - |
dc.contributor.author | Chae, Young Chan | - |
dc.contributor.author | Choi, Jang Hyun | - |
dc.contributor.author | Cocco, Lucio | - |
dc.contributor.author | Berggren, Per-Olof | - |
dc.contributor.author | Jang, Hyun-Jun | - |
dc.contributor.author | Suh, Pann-Ghill | - |
dc.date.accessioned | 2023-12-21T18:39:58Z | - |
dc.date.available | 2023-12-21T18:39:58Z | - |
dc.date.created | 2019-07-10 | - |
dc.date.issued | 2019-10 | - |
dc.description.abstract | PLC-β exerts biologic influences through GPCR. GPCRs are involved in regulating glucose-stimulated insulin secretion (GSIS). Previous studies have suggested that PLC-βs might play an important role in pancreatic β cells. However, because of a lack of the specific inhibitors of PLC-β isozymes and appropriate genetic models, the in vivo function of specific PLC-β isozymes in pancreatic β cells and their physiologic relevance in the regulation of insulin secretion have not been studied so far. The present study showed that PLC-β1 was crucial for β-cell function by generation of each PLC-β conditional knockout mouse. Mice lacking PLC-β1 in β cells exhibited a marked defect in GSIS, leading to glucose intolerance. In ex vivo studies, the secreted insulin level and Ca2+ response in Plcb1f/f; pancreas/duodenum homeobox protein 1 (Pdx1)-Cre recombinase–estrogen receptor T2 (CreERt2) islets was lower than those in the Plcb1f/f islets under the high-glucose condition. PLC-β1 led to potentiate insulin secretion via stimulation of particular Gq-protein–coupled receptors. Plcb1f/f; Pdx1-CreERt2 mice fed a high-fat diet developed more severe glucose intolerance because of a defect in insulin secretion. The present study identified PLC-β1 as an important molecule that regulates β cell insulin secretion and can be considered a candidate for therapeutic intervention in diabetes mellitus. | - |
dc.identifier.bibliographicCitation | FASEB JOURNAL, v.33, no.10, pp.10668 - 10679 | - |
dc.identifier.doi | 10.1096/fj.201802732rr | - |
dc.identifier.issn | 0892-6638 | - |
dc.identifier.scopusid | 2-s2.0-85072717353 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/26854 | - |
dc.identifier.url | https://www.fasebj.org/doi/10.1096/fj.201802732RR | - |
dc.identifier.wosid | 000489166300008 | - |
dc.language | 영어 | - |
dc.publisher | Federation of American Societies for Experimental Biology | - |
dc.title | Phospholipase C-β1 potentiates glucose-stimulated insulin secretion | - |
dc.type | Article | - |
dc.description.isOpenAccess | FALSE | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology; Biology; Cell Biology | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology | - |
dc.type.docType | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | GPCR | - |
dc.subject.keywordAuthor | GSIS | - |
dc.subject.keywordAuthor | intracellular Ca2+ | - |
dc.subject.keywordAuthor | PLC-β1 | - |
dc.subject.keywordPlus | PANCREATIC BETA-CELLS | - |
dc.subject.keywordPlus | PROTEIN-COUPLED RECEPTORS | - |
dc.subject.keywordPlus | 5-HYDROXYTRYPTAMINE RELEASE | - |
dc.subject.keywordPlus | DEPENDENT ACTIVATION | - |
dc.subject.keywordPlus | SIGNALING PATHWAYS | - |
dc.subject.keywordPlus | C ISOZYMES | - |
dc.subject.keywordPlus | CROSS-TALK | - |
dc.subject.keywordPlus | ISLETS | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | RESISTANCE | - |
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