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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2009;29:447.)
© 2009 American Heart Association, Inc.

Editorials

Getting Radical About Obesity

New Links Between Fat and Heart Disease

Matthias Barton; Elvira Haas; Indranil Bhattacharya

From the Departement für Innere Medizin, Klinik und Poliklinik für Innere Medizin, Universitätsspital Zürich, Switzerland.

Correspondence to Matthias Barton, MD, Professor, Departement für Innere Medizin, Klinik und Poliklinik für Innere Medizin, Universitë Zürich, Rämistrasse 100, CH-8091 Zürich, Switzerland. E-mail barton@usz.ch

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Visceral obesity has become the most frequent preventable condition accounting for diseases such as hypertension and diabetes, two of the major risk factors for coronary artery disease, stroke, and chronic renal failure.^1–3 Despite the awareness aiming to reduce the prevalence of obesity, the number of obese patients continues to rise and now includes even developing countries, and increasingly children are affected.^4,5 In fact, if this trend continues, 26 million children in Europe will be overweight or obese by the year 2010, rising by approximately 1.3 million per year.^5,6 The annual health costs related to obesity have been estimated close to 100 billion USD in the United States,^7,8 illustrating the enormous economic burden the disease obesity carries.

See accompanying article in ATVB 2009;29:239–245.

What are the mechanisms contributing to the high cardiovascular risk brought about by obesity? Obesity is a low-grade inflammatory condition⁹ and typically characterized by increase in visceral adipose tissue. Visceral fat is both a source and target of inflammatory cytokines and growth factors, which directly may affect preadipocyte differentiation via signaling cascades implicated in cell growth such as Ras-Raf-ERK-1/2.¹⁰ Adipose tissue also contains inflammatory cells, including cytokine-producing macrophages.⁹ In addition, adipocytes express a fully functional NADPH oxidase system maintaining local production of reactive oxygen species,¹¹ which in turn either work as signaling molecules or further stimulate production of growth factors implicated in adipogenesis.^12,13 Previous work has investigated effects of preadipocyte differentiation on expression of Nox4,¹⁴ a component of the vascular NADPH oxidase, and Mahadev et al demonstrated that . . . [Full Text of this Article]