Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9152
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dc.contributor.authorSoulis, Ten
dc.contributor.authorSastra, Sen
dc.contributor.authorThallas, Vickien
dc.contributor.authorMortensen, S Ben
dc.contributor.authorWilken, Men
dc.contributor.authorClausen, J Ten
dc.contributor.authorBjerrum, O Jen
dc.contributor.authorPetersen, Hen
dc.contributor.authorLau, Jen
dc.contributor.authorJerums, Georgeen
dc.contributor.authorBoel, Een
dc.contributor.authorCooper, Mark Een
dc.date.accessioned2015-05-15T22:07:53Z
dc.date.available2015-05-15T22:07:53Z
dc.date.issued1999-04-01en
dc.identifier.citationDiabetologia; 42(4): 472-9en
dc.identifier.govdoc10230652en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/9152en
dc.description.abstractPrevious studies in our laboratory have shown that the vascular changes in diabetes include hypertrophy of the mesenteric vasculature and that this process can be attenuated by the inhibition of advanced glycation with aminoguanidine. Since aminoguanidine can also act as an inhibitor of nitric oxide synthase, the effect of a novel inhibitor of advanced glycation end-products, formation that does not inhibit nitric oxide synthase, known as 2,3 diaminophenazine (2,3 DAP) was evaluated.Initially, in vitro assessment of the ability of 2,3 diaminophenazine to inhibit formation of advanced glycation products was performed. Subsequently, in vivo studies evaluating 2,3 diaminophenazine and aminoguanidine were carried out. Animals were followed for 3 weeks after induction of diabetes and randomised to no treatment, aminoguanidine or 2,3 diaminophenazine. Mesenteric vessels were weighed and advanced glycation end-products were measured by radioimmunoassay in vessel and kidney homogenates. In addition, these products were assessed in mesenteric vessels by immunohistochemistry.When compared with control animals, diabetes was associated with an increase in mesenteric vascular weight. Treatment of diabetic rats with aminoguanidine or 2,3 diaminophenazine resulted in attenuation of vascular hypertrophy. Both aminoguanidine and 2,3 diaminophenazine reduced the formation of advanced glycation end-products as measured by radioimmunoassay and as assessed immunohistochemically in these vessels. This reduction was also observed in the kidney.These data support the concept that the effects of aminoguanidine in reducing diabetes associated vascular hypertrophy are via inhibition of advanced glycation end-products dependent pathways.en
dc.language.isoenen
dc.subject.otherAnimalsen
dc.subject.otherDiabetes Mellitus, Experimental.complications.metabolismen
dc.subject.otherDiabetic Angiopathies.metabolismen
dc.subject.otherEnzyme Inductionen
dc.subject.otherGlycosylation End Products, Advanced.metabolismen
dc.subject.otherHypertrophy.prevention & controlen
dc.subject.otherMaleen
dc.subject.otherMesenteric Arteries.pathologyen
dc.subject.otherMesenteric Veins.pathologyen
dc.subject.otherMiceen
dc.subject.otherNitric Oxide Synthase.biosynthesisen
dc.subject.otherNitric Oxide Synthase Type IIen
dc.subject.otherPhenazines.pharmacologyen
dc.subject.otherRabbitsen
dc.subject.otherRadioimmunoassayen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.titleA novel inhibitor of advanced glycation end-product formation inhibits mesenteric vascular hypertrophy in experimental diabetes.en
dc.typeJournal Articleen
dc.identifier.journaltitleDiabetologiaen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg, Victoria, Australiaen
dc.identifier.doi10.1007/s001250051181en
dc.description.pages472-9en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/10230652en
dc.type.austinJournal Articleen
local.name.researcherJerums, George
item.fulltextWith Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.languageiso639-1en-
item.openairetypeJournal Article-
item.grantfulltextopen-
item.cerifentitytypePublications-
crisitem.author.deptEndocrinology-
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