on August 20, 2007
Published online before print August 20, 2007, doi: 10.1161/CIRCULATIONAHA.107.710509
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Submitted on April 19, 2007
From the National Heart, Lung, and Blood Institute’s Framingham Heart Study, Framingham, Mass (J.M. Massaro, R.S.V., M.G.L., J.M. Murabito, C.J.D., E.J.B., C.S.F.); Division of Endocrinology, Metabolism, and Diabetes, Brigham and Women’s Hospital and Harvard Medical School, Boston, Mass (K.M.P., C.S.F.); Boston University School of Public Health, Departments of Biostatistics (J.M. Massaro, M.G.L.) and Epidemiology (E.J.B.), Boston, Mass; Cardiac MR PET CT Program, Massachusetts General Hospital, Harvard Medical School, Boston, Mass (U.H.); Department of Cardiology (R.S.V., J.F.K., E.J.B.) and Preventive Medicine (R.S.V., E.J.B.), Whitaker Cardiovascular Institute (R.S.V., J.F.K., I.L., E.J.B.), Boston University School of Medicine, Boston, Mass; Semmelweis University, Budapest, Hungary (P.M.-H.); General Medicine Division, Massachusetts General Hospital, Harvard Medical School, Boston, Mass (J.B.M.); the Division of Cardiology, Massachusetts General Hospital and Harvard Medical School, Boston, Mass (C.J.D., S.K.); and Section of General Internal Medicine, Boston University School of Medicine, Boston, Mass (J.M. Murabito). * To whom correspondence should be addressed. E-mail: foxca{at}nhlbi.nih.gov.
Background—Excess adiposity is associated with greater systemic inflammation. Whether visceral adiposity is more proinflammatory than subcutaneous abdominal adiposity is unclear. Methods and Results—We examined the relations of abdominal subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT), assessed by multidetector computerized tomography, to circulating inflammatory and oxidative stress biomarkers in 1250 Framingham Heart Study participants (52% women; age 60±9 years). Biomarkers were examined in relation to increments of SAT and VAT after adjustment for age, sex, smoking, physical activity, menopause, hormone replacement therapy, alcohol, and aspirin use; additional models included body mass index and waist circumference. SAT and VAT were positively and similarly (with respect to strength of association) related to C-reactive protein, fibrinogen, intercellular adhesion molecule-1, interleukin-6, P-selectin, and tumor necrosis factor receptor-2 (multivariable model R2 0.06 to 0.28 [SAT] and 0.07 to 0.29 [VAT]). However, compared with SAT, VAT was more highly associated with urinary isoprostanes and monocyte chemoattractant protein-1 (SAT versus VAT comparison: isoprostanes, R2 0.07 versus 0.10, P=0.002; monocyte chemoattractant protein-1, R2 0.07 versus 0.08, P=0.04). When body mass index and waist circumference were added to the models, VAT remained significantly associated with only C-reactive protein (P=0.0003 for women; P=0.006 for men), interleukin-6 (P=0.01), isoprostanes (P=0.0002), and monocyte chemoattractant protein-1 (P=0.008); SAT only remained associated with fibrinogen (P=0.01). Conclusions—The present cross-sectional data support an association between both SAT and VAT with inflammation and oxidative stress. The data suggest that the contribution of visceral fat to inflammation may not be completely accounted for by clinical measures of obesity (body mass index and waist circumference).
Accepted on July 18, 2007
Visceral and Subcutaneous Adipose Tissue Volumes Are Cross-Sectionally Related to Markers of Inflammation and Oxidative Stress. The Framingham Heart Study
Karla M. Pou MD,
Key words: obesity • abdominal visceral fat • inflammation • computed tomography • epidemiology
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