Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9977
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dc.contributor.authorKooptiwut, Suwattaneeen
dc.contributor.authorKebede, Melkamen
dc.contributor.authorZraika, Sakenehen
dc.contributor.authorVisinoni, Sherleyen
dc.contributor.authorAston-Mourney, Kathrynen
dc.contributor.authorFavaloro, Jenny Men
dc.contributor.authorTikellis, Christosen
dc.contributor.authorThomas, Merlin Cen
dc.contributor.authorForbes, Josephine Men
dc.contributor.authorCooper, Mark Een
dc.contributor.authorDunlop, Marjorie Een
dc.contributor.authorProietto, Josephen
dc.contributor.authorAndrikopoulos, Sofianosen
dc.date.accessioned2015-05-15T23:16:46Z
dc.date.available2015-05-15T23:16:46Z
dc.date.issued2005-08-01en
dc.identifier.citationJournal of Molecular Endocrinology; 35(1): 39-48en
dc.identifier.govdoc16087720en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9977en
dc.description.abstractType 2 diabetes is characterized by islet dysfunction resulting in hyperglycemia, which can then lead to further deterioration in islet function. A possible mechanism for hyperglycemia-induced islet dysfunction is the accumulation of advanced glycation end products (AGE). The DBA/2 mouse develops pancreatic islet dysfunction when exposed to a high glucose environment and/or obesity-induced insulin resistance. To determine the biochemical cause of dysfunction, DBA/2 and C57BL/6 control islets were incubated in 11.1 mM or 40 mM glucose in the absence or presence of the AGE inhibitor aminoguanidine (AG) for 10 days. Basal (2.8 mM glucose) insulin release was increased in both DBA/2 and C57BL/6 islets incubated with 40 mM vs 11.1 mM glucose for 10 days. Chronic exposure to hyperglycemia decreased glucose (20 mM)-stimulated insulin secretion in DBA/2 but not in C57BL/6 islets. AG significantly increased fold-induced insulin release in high glucose cultured DBA/2 mouse islets, but did not affect C57BL/6 islet function. DBA/2 islet glucokinase was significantly reduced following 40 mM glucose culture, compared with 11.1 mM glucose cultured DBA/2 islets and 40 mM glucose cultured C57BL/6 islets. Incubation of islets with AG resulted in a normalization of DBA/2 islet glucokinase levels. In conclusion, chronic high glucose-induced increases in AGE can result in islet dysfunction and this is associated with reduced glucokinase levels in a mouse model with susceptibility to islet failure.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherBase Sequenceen
dc.subject.otherCell Survivalen
dc.subject.otherDNA.geneticsen
dc.subject.otherDiabetes Mellitus, Type 2.etiology.genetics.pathology.physiopathologyen
dc.subject.otherGlucokinase.metabolismen
dc.subject.otherGlucose.administration & dosage.pharmacologyen
dc.subject.otherGlucose Transporter Type 2en
dc.subject.otherGlycosylation End Products, Advanced.metabolismen
dc.subject.otherHexokinase.metabolismen
dc.subject.otherIn Vitro Techniquesen
dc.subject.otherInsulin.genetics.secretionen
dc.subject.otherIslets of Langerhans.drug effects.pathology.physiopathologyen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred C57BLen
dc.subject.otherMice, Inbred DBAen
dc.subject.otherMonosaccharide Transport Proteins.metabolismen
dc.subject.otherProinsulin.geneticsen
dc.subject.otherRNA, Messenger.genetics.metabolismen
dc.titleHigh glucose-induced impairment in insulin secretion is associated with reduction in islet glucokinase in a mouse model of susceptibility to islet dysfunction.en
dc.typeJournal Articleen
dc.identifier.journaltitleJournal of molecular endocrinologyen
dc.identifier.affiliationUniversity of Melbourne, Department of Medicine, Heidelberg Repatriation Hospital, 300 Waterdale Road, Heidelberg Heights, Victoria 3081, Australiaen
dc.identifier.doi10.1677/jme.1.01720en
dc.description.pages39-48en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/16087720en
dc.type.austinJournal Articleen
local.name.researcherProietto, Joseph
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptMedicine (University of Melbourne)-
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