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Tumour necrosis factor-alpha-induced glucose-stimulated insulin secretion inhibition in INS-1 cells is ascribed to a reduction of the glucose-stimulated Ca2+ influx.

DC Field Value Language
dc.contributor.authorKim, HE-
dc.contributor.authorChoi, SE-
dc.contributor.authorLee, SJ-
dc.contributor.authorLee, JH-
dc.contributor.authorLee, YJ-
dc.contributor.authorKang, SS-
dc.contributor.authorChun, J-
dc.contributor.authorKang, Y-
dc.date.accessioned2011-01-14T02:07:43Z-
dc.date.available2011-01-14T02:07:43Z-
dc.date.issued2008-
dc.identifier.issn0022-0795-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/1139-
dc.description.abstractThe present study was undertaken to determine how tumour necrosis factor-alpha (TNF-alpha) elicits the inhibition of glucose-stimulated insulin secretion (GSIS) in rat insulinoma cells (INS)-1 beta-cells. TNF-alpha pretreatment did not change the expression levels of insulin, PDX-1, glucose transporter 2, glucokinase, K(ATP) channels, Ca(2)(+) channels, and exocytotic molecules and, furthermore, did not reduce the glucose-stimulated ATP level. On the other hand, TNF-alpha reduced the glucose-stimulated influx of Ca(2)(+). The TNF-alpha treatment was thought to activate c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), and NF-kappaB inflammatory signals, since TNF-alpha increased phospho-JNK and phospho-p38 and reduced I kappaB levels. Inhibitors of these signaling pathways prevented the TNF-alpha-induced reduction of the Ca(2)(+) influx and GSIS. Overexpression of MEKK3, a possible mediator from the TNF-alpha receptor to the JNK/p38 and NK-kappaB signaling cascade, increased the levels of phospho-JNK, phospho-p38, and NF-kappaB, and reduced the glucose-stimulated Ca(2)(+) influx and GSIS. The reduction of the Ca(2)(+) influx and GSIS in MEKK3-overexpressing INS-1 cells was also prevented by inhibitors of JNK, p38, and NF-kappaB. These data demonstrate that TNF-alpha inhibits GSIS by reducing the glucose-stimulated Ca(2)(+) influx, possibly through the activation of JNK and p38 MAPK and NF-kappaB inflammatory signals. Thus, our findings suggest that the activation of stress and inflammatory signals can contribute to the inhibition of GSIS in the development of diabetes.-
dc.language.isoen-
dc.subject.MESHATP-Binding Cassette Transporters-
dc.subject.MESHAdenosine Triphosphate-
dc.subject.MESHAnimals-
dc.subject.MESHBiological Transport-
dc.subject.MESHCalcium-
dc.subject.MESHCalcium Channels-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHCell Survival-
dc.subject.MESHGene Expression-
dc.subject.MESHGlucokinase-
dc.subject.MESHGlucose-
dc.subject.MESHGlucose Transporter Type 2-
dc.subject.MESHHomeodomain Proteins-
dc.subject.MESHImmunoblotting-
dc.subject.MESHInsulin-
dc.subject.MESHInsulinoma-
dc.subject.MESHJNK Mitogen-Activated Protein Kinases-
dc.subject.MESHMAP Kinase Kinase Kinase 3-
dc.subject.MESHNF-kappa B-
dc.subject.MESHNitric Oxide Synthase Type II-
dc.subject.MESHPotassium Channels, Inwardly Rectifying-
dc.subject.MESHRadioimmunoassay-
dc.subject.MESHRats-
dc.subject.MESHReceptors, Drug-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHTrans-Activators-
dc.subject.MESHTumor Necrosis Factor-alpha-
dc.subject.MESHp38 Mitogen-Activated Protein Kinases-
dc.titleTumour necrosis factor-alpha-induced glucose-stimulated insulin secretion inhibition in INS-1 cells is ascribed to a reduction of the glucose-stimulated Ca2+ influx.-
dc.typeArticle-
dc.identifier.pmid18593820-
dc.identifier.urlhttp://joe.endocrinology-journals.org/cgi/pmidlookup?view=long&pmid=18593820-
dc.contributor.affiliatedAuthor최, 성이-
dc.contributor.affiliatedAuthor강, 엽-
dc.type.localJournal Papers-
dc.identifier.doi10.1677/JOE-08-0131-
dc.citation.titleThe Journal of endocrinology-
dc.citation.volume198-
dc.citation.number3-
dc.citation.date2008-
dc.citation.startPage549-
dc.citation.endPage560-
dc.identifier.bibliographicCitationThe Journal of endocrinology, 198(3). : 549-560, 2008-
dc.identifier.eissn1479-6805-
dc.relation.journalidJ000220795-
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Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
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