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dc.contributor.authorZraika, Sen
dc.contributor.authorAston-Mourney, Kathrynen
dc.contributor.authorLaybutt, D Ren
dc.contributor.authorKebede, Men
dc.contributor.authorDunlop, Mark Een
dc.contributor.authorProietto, Josephen
dc.contributor.authorAndrikopoulos, Sofianosen
dc.date.accessioned2015-05-15T23:29:10Z
dc.date.available2015-05-15T23:29:10Z
dc.date.issued2006-03-29en
dc.identifier.citationDiabetologia 2006; 49(6): 1254-63en
dc.identifier.govdoc16570159en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10132en
dc.description.abstractWe determined whether high-glucose-induced beta cell dysfunction is associated with oxidative stress in the DBA/2 mouse, a mouse strain susceptible to islet failure.Glucose- and non-glucose-mediated insulin secretion from the islets of DBA/2 and control C57BL/6 mice was determined following a 48-h exposure to high glucose. Flux via the hexosamine biosynthesis pathway was assessed by determining O-glycosylated protein levels. Oxidative stress was determined by measuring hydrogen peroxide levels and the expression of anti-oxidant enzymes.Exposure to high glucose levels impaired glucose-stimulated insulin secretion in DBA/2 islets but not C57BL/6 islets, and this was associated with reduced islet insulin content and lower ATP levels than in C57BL/6 islets. Exposure of islets to glucosamine for 48 h mimicked the effects of high glucose on insulin secretion in the DBA/2 islets. High glucose exposure elevated O-glycosylated proteins; however, this occurred in islets from both strains, excluding a role for O-glycosylation in the impairment of DBA/2 insulin secretion. Additionally, both glucosamine and high glucose caused an increase in hydrogen peroxide in DBA/2 islets but not in C57BL/6 islets, an effect prevented by the antioxidant N-acetyl-L: -cysteine. Interestingly, while glutathione peroxidase and catalase expression was comparable between the two strains, the antioxidant enzyme manganese superoxide dismutase, which converts superoxide to hydrogen peroxide, was increased in DBA/2 islets, possibly explaining the increase in hydrogen peroxide levels.Chronic high glucose culture caused an impairment in glucose-stimulated insulin secretion in DBA/2 islets, which have a genetic predisposition to failure, and this may be the result of oxidative stress.en
dc.language.isoenen
dc.subject.otherAdenosine Triphosphate.metabolismen
dc.subject.otherAnimalsen
dc.subject.otherCell Culture Techniquesen
dc.subject.otherCell Survivalen
dc.subject.otherDNA Primersen
dc.subject.otherGene Expression Regulationen
dc.subject.otherGlucose.pharmacologyen
dc.subject.otherGlycosylationen
dc.subject.otherHydrogen Peroxide.analysisen
dc.subject.otherInsulin.secretionen
dc.subject.otherIslets of Langerhans.cytology.drug effects.secretionen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred C57BLen
dc.subject.otherMice, Inbred DBA.geneticsen
dc.subject.otherOxidative Stress.geneticsen
dc.subject.otherPolymerase Chain Reaction.methodsen
dc.titleThe influence of genetic background on the induction of oxidative stress and impaired insulin secretion in mouse islets.en
dc.typeJournal Articleen
dc.identifier.journaltitleDiabetologiaen
dc.identifier.affiliationDepartment of Medicine (AH/NH), University of Melbourne, Heidelberg Repatriation Hospital, Heidelberg Heights, VIC 3081, Australiaen
dc.identifier.doi10.1007/s00125-006-0212-9en
dc.description.pages1254-63en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/16570159en
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