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      Impact of Angiotensin II Receptor Blocker on Plasma Levels of Adiponectin and Advanced Oxidation Protein Products in Peritoneal Dialysis Patients

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          Abstract

          Background: Oxidative stress and adipocytokines are reported to contribute to the pathogenesis of atherosclerosis. Though the inhibition of the renin-angiotensin system is known to have beneficial effects on atherosclerosis, the exact mechanisms for this remain to be clarified. The aim of this study was to determine the effects of angiotensin II receptor blockers (ARB) on the oxidative stress and adipocytokines in peritoneal dialysis patients. Methods: Candesartan (8 mg/day), an ARB, was administered for 3 months to 8 nondiabetic patients on peritoneal dialysis. Plasma levels of advanced oxidation protein products (AOPP) and adiponectin were measured before and 3 months after candesartan administration, and 3 months after discontinuation. Results: Plasma AOPP level decreased from 377.5 to 305.6 µmol/l (p < 0.05) following the administration of candesartan and returned to 394.6 µmol/l (p < 0.05) by 3 months after the discontinuation of the drug. Plasma adiponectin level increased from 12.5 to 18.8 µg/ml (p < 0.05) by candesartan and decreased again to 14.4 µg/ml (p < 0.05) after discontinuation. There was a significant inverse relationship between changes in plasma level of adiponectin and AOPP (r = – 0.888, p < 0.01). Conclusion: Candesartan increases plasma adiponectin level in association with the reduction of oxidative stress in peritoneal dialysis patients. Candesartan may be useful in preventing atherosclerosis in peritoneal dialysis patients.

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          Most cited references 18

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          Adiponectin reduces atherosclerosis in apolipoprotein E-deficient mice.

          Dysregulation of adipocyte-derived bioactive molecules plays an important role in the development of atherosclerosis. We previously reported that adiponectin, an adipocyte-specific plasma protein, accumulated in the injured artery from the plasma and suppressed endothelial inflammatory response and vascular smooth muscle cell proliferation, as well as macrophage-to-foam cell transformation in vitro. The current study investigated whether the increased plasma adiponectin could actually reduce atherosclerosis in vivo. Apolipoprotein E-deficient mice were treated with recombinant adenovirus expressing human adiponectin (Ad-APN) or beta-galactosidase (Ad-betagal). The plasma adiponectin levels in Ad-APN-treated mice increased 48 times as much as those in Ad-betagal treated mice. On the 14th day after injection, the lesion formation in aortic sinus was inhibited in Ad-APN-treated mice by 30% compared with Ad-betagal-treated mice (P<0.05). In the lesions of Ad-APN-treated mice, the lipid droplets became smaller compared with Ad-betagal-treated mice (P<0.01). Immunohistochemical analyses demonstrated that the adenovirus-mediated adiponectin migrate to foam cells in the fatty streak lesions. The real-time quantitative polymerase chain reaction revealed that Ad-APN treatment significantly suppressed the mRNA levels of vascular cell adhesion molecule-1 by 29% and class A scavenger receptor by 34%, and tended to reduce levels of tumor necrosis factor-alpha without affecting those of CD36 in the aortic tissue. These findings documented for the first time that elevated plasma adiponectin suppresses the development of atherosclerosis in vivo.
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            Reciprocal association of C-reactive protein with adiponectin in blood stream and adipose tissue.

            High-sensitive C-reactive protein (hs-CRP) is a well-known risk factor for coronary artery disease (CAD). Recently, we have demonstrated that adiponectin served as an antiatherogenic plasma protein which was secreted specifically from adipocytes. The present study investigated the association between adiponectin and CRP in the blood stream and adipose tissue. We studied a total of 101 male patients, 71 of whom had angiographically documented coronary atherosclerosis. As a control group, 30 patients with normal coronary angiogram were included. The plasma hs-CRP levels were negatively correlated with the plasma adiponectin levels (r=-0.29, P<0.01). The plasma adiponectin concentrations were significantly lower and the hs-CRP levels were significantly higher in the CAD patients compared with control subjects. The mRNA levels of CRP and adiponectin were analyzed by quantitative real-time polymerase chain reaction method. We found that the CRP mRNA was expressed in human adipose tissue. A significant inverse correlation was observed between the CRP and adiponectin mRNA levels in human adipose tissue (r=-0.89, P<0.01). In addition, the CRP mRNA level of white adipose tissue in adiponectin deficient mice was higher than that of wild-type mice. The reciprocal association of adiponectin and CRP levels in both human plasma and adipose tissue might participate in the development of atherosclerosis.
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              PPAR  Ligands Increase Expression and Plasma Concentrations of Adiponectin, an Adipose-Derived Protein

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                Author and article information

                Journal
                BPU
                Blood Purif
                10.1159/issn.0253-5068
                Blood Purification
                S. Karger AG
                0253-5068
                1421-9735
                2006
                December 2006
                21 December 2006
                : 24
                : 5-6
                : 445-450
                Affiliations
                aRenal Division, Department of Internal Medicine, Iwata City Hospital, Iwata, bDepartment of Clinical Nutrition, School of Food and Nutritional Sciences, University of Shizuoka, Shizuoka, and cFirst Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan
                Article
                95361 Blood Purif 2006;24:445–450
                10.1159/000095361
                16940715
                © 2006 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 1, Tables: 3, References: 21, Pages: 6
                Product
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/95361
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