(Circulation. 2007;115:946-948.)
© 2007 American Heart Association, Inc.
Editorial |
From Cardiovascular Research, Institute of Physiology (C.M.M.), and the Zürich Center for Integrative Human Physiology (C.M.M., C.H.), Institute of Physiology (C.H.), University of Zürich; and the Clinic of Cardiology, CardioVascular Center, University Hospital Zürich (C.M.M.), Zürich, Switzerland.
Correspondence to Dr Christian M. Matter, Cardiovascular Research, Institute of Physiology, University of Zürich, and Cardiology, CardioVascular Center, University Hospital Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland. E-mail cmatter@physiol.unizh.ch
Key Words: Editorials inflammation obesity RANTES adipose tissue
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
For a long time, white adipose tissue (WAT) has been regarded as an inert tissue for energy storage. With the rapidly rising incidence of the components of the metabolic syndromeobesity, diabetes mellitus type II, and hypertensionin the industrialized world, these diseases have attracted increasing attention in research and health politics. In parallel, WAT was recognized as an active endocrine and paracrine organ that plays an important role in the metabolic syndrome.1
Article p 1029
Various studies within the past decade indicated that WAT in obesity is characterized by a chronic low-grade inflammation with secretion of inflammatory cytokines and chemokines (see the Figure). Tumor necrosis factor-
was identified as the first molecular link between inflammation and obesity by Hotamisligil and coworkers: Expression of this cytokine was increased in WAT of obese mice2 and correlated with obesity-induced insulin resistance.3 Interleukin-6 (IL-6) is another cytokine critically involved in the pathogenesis of obesity and insulin resistance. The serum levels of IL-6 positively correlate with obesity in humans and predict the risk of development of insulin resistance and diabetes mellitus type 2.4 IL-6 is produced by a variety of metabolic tissues that include WAT, hepatocytes, ß-cells, and skeletal muscle. Thus, circulating IL-6 could mediate a crosstalk between these organs that results in a downward spiral toward systemic insulin resistance and decreased insulin secretion.5 Furthermore, obesity was found to be associated with macrophage accumulation in murine and human WAT.6 Chemokines such as CCL2/monocyte chemoattractant protein-1 (MCP-1) and CCL3/macrophage inflammatory protein-1
were reported to be increased
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