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Mediators of Inflammation
Volume 2010, Article ID 841343, 12 pages
Research Article

The Effect of Chronic Candesartan Therapy on the Metabolic Profile and Renal Tissue Cytokine Levels in the Obese Zucker Rat

1Division of Endocrinology and Metabolism, Department of Medicine, Georgetown University, Washington, DC 20057, USA
2Laboratory of Immunoregulation, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA

Received 2 October 2009; Revised 27 January 2010; Accepted 5 March 2010

Academic Editor: Giuseppe Matarese

Copyright © 2010 Carolyn M. Ecelbarger et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The effect of candesartan, an angiotensin-II type-1 receptor antagonist, on the metabolic profile and renal inflammation is unclear. We evaluated this relationship by feeding male lean (LZ) and obese (OZ) Zucker rats chow or chow with candesartan (23.5 mg/ ) for 14 weeks ( –8/treatment/body type). Candesartan reduced serum triglycerides, plasma creatinine, urine albumin, and renal cortical collagen and glycogen deposition in the OZ. An ELISA-based cytokine array revealed that candesartan normalized elevated renal interleukin (IL) 1- and monocyte chemoattractant protein-1 (MCP-1) levels in OZ. Nonetheless, candesartan impaired glucose tolerance, and did not lower blood insulin or glucose levels. Moreover, renal IL-1 , -2, -4, -6 and -10 tumor necrosis factor- , interferon- , were significantly reduced in OZ relative to LZ, and increased by candesartan. Furthermore, candesartan increased growth-regulated oncogene, transforming growth factor- 1 and IL-18 in OZ kidneys to a level higher than LZ or untreated OZ. Candesartan did not affect renal cytokine levels in LZ. Overall, candesartan attenuated renal disease and improved renal function in OZ, despite mixed effects on metabolic factors and cytokines. Reduced plasma triglycerides and/or renal MCP-1 and IL-1 may have had a role in this protection. However, these effects were clearly independent of any improvement in glucose tolerance.