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Human epicardial adipose tissue expresses a pathogenic profile of adipocytokines in patients with cardiovascular disease

By Adam R. Baker, Nancy Fernandez da Silva, David W. Quinn, A. L. (Alison L.) Harte, Domenico Pagano, Robert S. Bonser, Sudhesh Kumar and P. G. (Philip G.) McTernan

Abstract

Introduction: Inflammation contributes to cardiovascular disease and is exacerbated with\ud increased adiposity, particularly omental adiposity; however, the role of epicardial fat is poorly\ud understood.\ud Methods: For these studies the expression of inflammatory markers was assessed in epicardial fat\ud biopsies from coronary artery bypass grafting (CABG) patients using quantitative RT-PCR. Further,\ud the effects of chronic medications, including statins, as well as peri-operative glucose, insulin and\ud potassium infusion, on gene expression were also assessed. Circulating resistin, CRP, adiponectin\ud and leptin levels were determined to assess inflammation.\ud Results: The expression of adiponectin, resistin and other adipocytokine mRNAs were\ud comparable to that in omental fat. Epicardial CD45 expression was significantly higher than control\ud depots (p < 0.01) indicating significant infiltration of macrophages. Statin treated patients showed\ud significantly lower epicardial expression of IL-6 mRNA, in comparison with the control abdominal\ud depots (p < 0.001). The serum profile of CABG patients showed significantly higher levels of both\ud CRP (control: 1.28 ± 1.57 μg/mL vs CABG: 9.11 ± 15.7 μg/mL; p < 0.001) and resistin (control:\ud 10.53 ± 0.81 ng/mL vs CABG: 16.8 ± 1.69 ng/mL; p < 0.01) and significantly lower levels of\ud adiponectin (control: 29.1 ± 14.8 μg/mL vs CABG: 11.9 ± 6.0 μg/mL; p < 0.05) when compared to\ud BMI matched controls.\ud Conclusion: Epicardial and omental fat exhibit a broadly comparable pathogenic mRNA profile,\ud this may arise in part from macrophage infiltration into the epicardial fat. This study highlights that\ud chronic inflammation occurs locally as well as systemically potentially contributing further to the\ud pathogenesis of coronary artery disease

Topics: RC
Publisher: Biomed central
Year: 2006
OAI identifier: oai:wrap.warwick.ac.uk:141

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