Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/10808
Full metadata record
DC FieldValueLanguage
dc.contributor.authorZulli, Anthonyen
dc.contributor.authorLau, Ezaen
dc.contributor.authorWijaya, Bagus P Pen
dc.contributor.authorJin, Xinen
dc.contributor.authorSutarga, Komangen
dc.contributor.authorSchwartz, Grace Den
dc.contributor.authorLearmont, Jonathonen
dc.contributor.authorWookey, Peter Jen
dc.contributor.authorZinellu, Angeloen
dc.contributor.authorCarru, Ciriacoen
dc.contributor.authorHare, David Len
dc.date.accessioned2015-05-16T00:22:42Z
dc.date.available2015-05-16T00:22:42Z
dc.date.issued2009-04-27en
dc.identifier.citationHypertension 2009; 53(6): 1017-22en
dc.identifier.govdoc19398656en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/10808en
dc.description.abstractWe sought to determine whether taurine could specifically protect against coronary artery disease during an atherogenic diet and whether taurine affects the lipid profile, metabolites of methionine, and endothelial atherogenic systems. Rabbits were fed one of the following diets for 4 weeks: (1) control diet; (2) 0.5% cholesterol+1.0% methionine; or (3) 0.5% cholesterol+1.0% methionine+2.5% taurine. Endothelial function was examined, and the left main coronary artery atherosclerosis was quantified by stereology and semiquantitative immunohistochemistry to determine the endothelial expression of proteins related to the NO, renin-angiotensin, endoplasmic reticulum, and oxidative stress systems, as well as apoptosis. Taurine normalized hyperhomocysteinemia (P<0.05) and significantly reduced hypermethioninemia (P<0.05) but not lipidemia. The intima:media ratio was reduced by 28% (P=0.034), and atherosclerosis was reduced by 64% (P=0.012) and endothelial cell apoptosis by 30% (P<0.01). Endothelial cell CCAAT/enhancer binding protein homologous protein was normalized (P<0.05). Taurine failed to improve hyperlipidemia, endothelial function, or endothelial proteins related to the NO, renin-angiotensin, and oxidative stress systems. Taurine reduces left main coronary artery wall pathology associated with decreased plasma total homocysteine, methionine, apoptosis, and normalization of CCAAT/enhancer binding protein homologous protein. These results elucidate the antiapoptotic and antiatherogenic properties of taurine, possibly via normalization of endoplasmic reticulum stress.en
dc.language.isoenen
dc.subject.otherAnalysis of Varianceen
dc.subject.otherAnimalsen
dc.subject.otherApoptosis.drug effectsen
dc.subject.otherCCAAT-Binding Factor.drug effects.metabolismen
dc.subject.otherCoronary Artery Disease.pathology.prevention & controlen
dc.subject.otherDiet, Atherogenicen
dc.subject.otherDietary Supplementsen
dc.subject.otherDisease Models, Animalen
dc.subject.otherEndothelium, Vascular.drug effects.pathologyen
dc.subject.otherHomocysteine.blooden
dc.subject.otherHyperlipidemias.physiopathologyen
dc.subject.otherMaleen
dc.subject.otherMethionine.pharmacologyen
dc.subject.otherNitric Oxide.metabolismen
dc.subject.otherOxidative Stressen
dc.subject.otherProbabilityen
dc.subject.otherRabbitsen
dc.subject.otherRandom Allocationen
dc.subject.otherReference Valuesen
dc.subject.otherSensitivity and Specificityen
dc.subject.otherTaurine.pharmacologyen
dc.titleHigh dietary taurine reduces apoptosis and atherosclerosis in the left main coronary artery: association with reduced CCAAT/enhancer binding protein homologous protein and total plasma homocysteine but not lipidemia.en
dc.typeJournal Articleen
dc.identifier.journaltitleHypertensionen
dc.identifier.affiliationDepartments of Cardiology, University of Melbourne, Austin Health, Heidelberg, Australia. azulli@unimelb.edu.auen
dc.identifier.doi10.1161/HYPERTENSIONAHA.109.129924en
dc.description.pages1017-22en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/19398656en
Appears in Collections:Journal articles

Files in This Item:
There are no files associated with this item.


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.