Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/104031
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dc.contributor.authorBarden, A.-
dc.contributor.authorO Callaghan, N.-
dc.contributor.authorBurke, V.-
dc.contributor.authorMas, E.-
dc.contributor.authorBeilin, L.J.-
dc.contributor.authorFenech, M.-
dc.contributor.authorIrish, A.B.-
dc.contributor.authorWatts, G.F.-
dc.contributor.authorPuddey, I.B.-
dc.contributor.authorHuang, R.C.-
dc.contributor.authorMori, T.A.-
dc.date.issued2016-
dc.identifier.citationNutrients, 2016; 8(3):1-11-
dc.identifier.issn2072-6643-
dc.identifier.issn2072-6643-
dc.identifier.urihttp://hdl.handle.net/2440/104031-
dc.description.abstractDNA telomere shortening associates with the age-related increase cardiovascular disease (CVD) risk. Reducing oxidative stress, could modify telomere erosion during cell replication, and CVD risk in patients with chronic kidney disease (CKD). The effect of n-3 fatty acids and coenzyme Q10 (CoQ) on telomere length was studied in a double-blind placebo-controlled trial in CKD. Eighty-five CKD patients were randomized to: n-3 fatty acids (4 g); CoQ (200 mg); both supplements; or control (4 g olive oil), daily for 8 weeks. Telomere length was measured in neutrophils and peripheral blood mononuclear cells (PBMC) at baseline and 8 weeks, with and without correction for cell counts. Main and interactive effects of n-3 fatty acids and CoQ on telomere length were assessed adjusting for baseline values. F2-isoprostanes were measured as markers of oxidative stress. There was no effect of n-3 fatty acids or CoQ on neutrophil or PBMC telomere length. However, telomere length corrected for neutrophil count was increased after n-3 fatty acids (p = 0.015). Post-intervention plasma F2-isoprostanes were negative predictors of post-intervention telomere length corrected for neutrophil count (p = 0.025).The effect of n-3 fatty acids to increased telomere length corrected for neutrophil count may relate to reduced oxidative stress and increased clearance of neutrophils with shorter telomeres from the circulation. This may be a novel mechanism of modifying CVD risk in CKD patients.-
dc.description.statementofresponsibilityAnne Barden, Nathan O'Callaghan, Valerie Burke, Emile Mas, Lawrence J. Beilin, Michael Fenech, Ashley B. Irish, Gerald F. Watts, Ian B. Puddey, Rae-Chi Huang and Trevor A. Mori-
dc.language.isoen-
dc.publisherMDPI AG-
dc.rights© 2016 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license (http://creativecommons.org/licenses/by/4.0/).-
dc.source.urihttp://dx.doi.org/10.3390/nu8030175-
dc.subjectneutrophils; telomere length; oxidative stress; n-3 fatty acids; coenzyme Q10-
dc.titlen-3 fatty acid supplementation and leukocyte telomere length in patients with chronic kidney disease-
dc.typeJournal article-
dc.identifier.doi10.3390/nu8030175-
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/303151-
dc.relation.granthttp://purl.org/au-research/grants/nhmrc/1010495-
pubs.publication-statusPublished-
dc.identifier.orcidMas, E. [0000-0003-2848-9613]-
dc.identifier.orcidFenech, M. [0000-0002-8466-0991]-
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