Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/13549
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dc.contributor.authorSoulis, Ten
dc.contributor.authorCooper, Mark Een
dc.contributor.authorSastra, Sen
dc.contributor.authorThallas, Vickien
dc.contributor.authorPanagiotopoulos, Siannaen
dc.contributor.authorBjerrum, O Jen
dc.contributor.authorJerums, Georgeen
dc.date.accessioned2015-05-16T03:25:34Z-
dc.date.available2015-05-16T03:25:34Z-
dc.date.issued1997-10-01en
dc.identifier.citationDiabetologia; 40(10): 1141-51en
dc.identifier.govdoc9349594en
dc.identifier.otherPUBMEDen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/13549en
dc.description.abstractAdvanced glycation end products (AGEs) have previously been shown to be increased in the diabetic kidney. Aminoguanidine, an inhibitor of advanced glycation, has been shown to attenuate the development of AGEs as well as the progression of renal disease in experimental diabetes. However, the precise mechanisms through which aminoguanidine acts remain to be elucidated since it is also able to act as an inhibitor of nitric oxide synthase (NOS). This study has therefore compared the effects of aminoguanidine with the effects of two other inhibitors of NOS, L-NAME and methylguanidine, on the development of experimental diabetic nephropathy. Diabetic rats were randomised to receive no treatment, aminoguanidine (1 g/l in drinking water), L-NAME (5 mg/l in drinking water) or methylguanidine (1 g/l in drinking water). Diabetic rats had increased levels of albuminuria and urinary nitrite/nitrate excretion when compared to control rats. Renal AGEs measured by fluorescence as well as by a carboxymethyllysine reactive radioimmunoassay, were elevated in diabetic rats. No changes in inducible NOS (iNOS) protein expression were detected in experimental diabetes nor did aminoguanidine affect iNOS expression. Aminoguanidine did not affect blood glucose or HbA1c but it did prevent increases in albuminuria, urinary nitrites/nitrates and renal AGE levels as measured by fluorescence and radioimmunoassay. L-NAME and methylguanidine did not retard the development of albuminuria, nor did they prevent increases in renal AGE levels, as assessed by fluorescence. However, these treatments did prevent increases in AGEs, as measured by radioimmunoassay. This study indicates that the renoprotective effect of aminoguanidine in experimental diabetes cannot be reproduced by L-NAME or methylguanidine. It is likely that the effect of aminoguanidine is mediated predominantly by decreased AGE formation rather than via NOS inhibition. It also raises the possibility that inhibition of fluorescent AGE formation may be more renoprotective than inhibition of the formation of carboxymethyllysine-containing AGEs.en
dc.language.isoenen
dc.subject.otherAdministration, Oralen
dc.subject.otherAlbuminuria.metabolism.urineen
dc.subject.otherAnimalsen
dc.subject.otherCohort Studiesen
dc.subject.otherDiabetes Mellitus, Experimental.immunology.pathology.urineen
dc.subject.otherEnzyme Inhibitors.administration & dosage.pharmacologyen
dc.subject.otherGlycosylation End Products, Advanced.immunology.metabolism.urineen
dc.subject.otherGuanidines.administration & dosage.pharmacologyen
dc.subject.otherImmunohistochemistryen
dc.subject.otherKidney Glomerulus.drug effects.immunology.metabolism.pathologyen
dc.subject.otherMaleen
dc.subject.otherMethylguanidine.administration & dosage.pharmacologyen
dc.subject.otherNG-Nitroarginine Methyl Ester.administration & dosage.pharmacologyen
dc.subject.otherNitrates.urineen
dc.subject.otherNitric Oxide Synthase.antagonists & inhibitorsen
dc.subject.otherNitrites.urineen
dc.subject.otherRandom Allocationen
dc.subject.otherRatsen
dc.subject.otherRats, Sprague-Dawleyen
dc.subject.otherTime Factorsen
dc.titleRelative contributions of advanced glycation and nitric oxide synthase inhibition to aminoguanidine-mediated renoprotection in diabetic ratsen
dc.typeJournal Articleen
dc.identifier.journaltitleDiabetologiaen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre (Repatriation Campus), West Heidelberg, Australiaen
dc.identifier.doi10.1007/s001250050799en
dc.description.pages1141-51en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/9349594en
dc.identifier.orcid0000-0002-0845-0001-
dc.type.austinJournal Articleen
local.name.researcherJerums, George
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.fulltextWith Fulltext-
item.grantfulltextopen-
item.languageiso639-1en-
item.openairetypeJournal Article-
crisitem.author.deptOffice for Research-
crisitem.author.deptEndocrinology-
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