Startseite Plasma advanced glycation end products (AGEs) and NF-κB activity are independent determinants of diastolic and pulse pressure
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Plasma advanced glycation end products (AGEs) and NF-κB activity are independent determinants of diastolic and pulse pressure

  • Karly C. Sourris , Jasmine G. Lyons , Sonia L. Dougherty , Vibhasha Chand , Nora E. Straznicky , Markus P. Schlaich , Mariee T. Grima , Mark E. Cooper , Bronwyn A. Kingwell , Maximilian P.J. de Courten , Josephine M. Forbes und Barbora de Courten EMAIL logo
Veröffentlicht/Copyright: 23. März 2013
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Abstract

Background: High levels of circulating advanced glycation end products (AGEs) can initiate chronic low-grade activation of the immune system (CLAIS) with each of these factors independently associated with cardiovascular (CV) morbidity and mortality. Therefore, our objective was to characterize the relationship between serum AGEs, CLAIS and other risk factors for CV disease in normotensive non-diabetic individuals.

Methods: We measured body mass index (BMI), waist-to-hip ratio (WHR), blood pressure, lipid and glucose profile in 44 non-diabetic volunteers (17 female, 27 males). Carboxymethyl-lysine (CML) was measured by ELISA as a marker for circulating AGEs and NF-κB p65 activity as an inflammatory marker by DNA-binding in peripheral blood mononuclear cells lysates (PBMC).

Results: Plasma CML concentrations were related to diastolic blood pressure (r=−0.51, p<0.01) independently of age, sex, BMI and WHR (p<0.05). Diastolic blood pressure was also related to NF-κB activity in PBMC (r=0.47, p<0.01) before and after adjustment for age, sex, BMI and WHR (p<0.05). Plasma CML concentrations were related to the pulse pressure before (r=0.42; p<0.05) and after adjustment for age, sex, BMI and waist (p<0.05). Neither CML nor NF-κB activity were related to systolic blood pressure (both p=ns). Plasma CML concentrations were not associated with plasma lipid or glucose concentrations (all p=ns).

Conclusions: Plasma AGE levels and NF-κB activity in PBMC were independent determinants of diastolic and pulse pressure in healthy normotensive individuals. This association suggests a role for AGEs in the etiology of hypertension, possibly via the initiation of CLAIS and aortic stiffening.


Corresponding author: A/Prof. Barbora de Courten, MD, PhD, MPH, FRACP, Baker IDI Heart and Diabetes Institute, 75 Commercial Rd, Melbourne, 3004, VIC, Australia, Phone: +61 3 85321353, Fax: +61 3 85321111, E-mail:

We wish to thank all volunteers for their participation in the study. This research was supported by Bennelong foundation, Cardiovascular lipid grant, National Health and Medical Research Council of Australia (NHMRC) and Diabetes Australia Research Trust Millennium Award and the Victorian Government’s Operational Infrastructure Support Program. BdC, JMF, BK, MEC, MS are all fellows of the NHMRC of Australia. KCS is supported by a Viertel Diabetes Australia Research Trust Fellowship. No sponsor had any role in the study design, data collection, data analysis, data interpretation, or writing of the manuscript.

Conflict of interest statement

Authors’ conflict of interest disclosure: The authors stated that there are no conflicts of interest regarding the publication of this article.

Research funding: None declared.

Employment or leadership: None declared.

Honorarium: None declared.

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Received: 2012-12-5
Accepted: 2013-2-14
Published Online: 2013-03-23
Published in Print: 2014-01-01

©2014 by Walter de Gruyter Berlin Boston

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