Volume 115, Issue 5 , Pages 911-919, May 2005
Adipose tissue, adipokines, and inflammation
This activity is available for CME credit. See page 28A for important information.White adipose tissue is no longer considered an inert tissue mainly devoted to energy storage but is emerging as an active participant in regulating physiologic and pathologic processes, including immunity and inflammation. Macrophages are components of adipose tissue and actively participate in its activities. Furthermore, cross-talk between lymphocytes and adipocytes can lead to immune regulation. Adipose tissue produces and releases a variety of proinflammatory and anti-inflammatory factors, including the adipokines leptin, adiponectin, resistin, and visfatin, as well as cytokines and chemokines, such as TNF-α, IL-6, monocyte chemoattractant protein 1, and others. Proinflammatory molecules produced by adipose tissue have been implicated as active participants in the development of insulin resistance and the increased risk of cardiovascular disease associated with obesity. In contrast, reduced leptin levels might predispose to increased susceptibility to infection caused by reduced T-cell responses in malnourished individuals. Altered adipokine levels have been observed in a variety of inflammatory conditions, although their pathogenic role has not been completely clarified.
Key words: Obesity, inflammation, immunity, cytokines, adipokines, insulin resistance, adipose tissue
Abbreviations used: BMI, Body mass index, CRP, C-reactive protein, CVD, Cardiovascular disease, FIZZ, Found in inflammatory zone, IBD, Inflammatory bowel disease, ICAM-1, Intracellular adhesion molecule 1, MCP-1, Monocyte chemoattractant protein 1, NF-κB, Nuclear factor κB, PBEF, Pre-B-cell colony-enhancing factor, RA, Rheumatoid arthritis, RELM, Resistin-like molecule, WAT, White adipose tissue
Series editors: William T. Shearer, MD, PhD, Lanny J. Rosenwasser, MD, and Bruce S. Bochner, MDSupported by National Institutes of Health grant DK-061483.Disclosure of potential conflict of interest: G. Fantuzzi—none disclosed.
PII: S0091-6749(05)00417-3
doi:10.1016/j.jaci.2005.02.023
© 2005 American Academy of Allergy, Asthma and Immunology. Published by Elsevier Inc. All rights reserved.
Volume 115, Issue 5 , Pages 911-919, May 2005
