The evolving role of inflammation in obesity and the metabolic syndrome

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ID: 116283
1970
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Abstract
Advances in adipose tissue biology over the past 10 years have led to an improved understanding of the mechanisms linking obesity with the metabolic syndrome and other complications. Obesity is characterized by a chronic, systemic low-grade state of inflammation. Biomarkers of inflammation, such as the leukocyte count, tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and C-reactive protein, are increased in obesity, associated with insulin resistance, and predict the development of type 2 diabetes and cardiovascular disease. It is now clear that the adipocyte is an active participant in the generation of the inflammatory state in obesity. Adipocytes secrete a variety of cytokines, including IL-6 and TNF-α, that promote inflammation. Moreover, recent studies suggest that obesity is associated with an increase in adipose tissue macrophages, which also participate in the inflammatory process through the elaboration of cytokines. An improved understanding of the role of adipose tissue in the activation of inflammatory pathways may suggest novel treatment and prevention strategies aimed at reducing obesity-associated morbidities and mortality.
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lee1970currentthe Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Yong-Ho Lee;Richard E. Pratley;Yong-Ho Lee;Richard E. Pratley;
Journal current diabetes reports
Year 1970
DOI
doi:10.1007/s11892-005-0071-7
URL
http://dx.doi.org/10.1007/s11892-005-0071-7
Keywords
Diabetes National Center for Biotechnology Information NCBI NLM MEDLINE review humans pubmed abstract nih national institutes of health national library of medicine diabetes mellitus inflammation / physiopathology* metabolic syndrome / physiopathology* insulin resistance / physiology type 2 / physiopathology obesity / physiopathology* pmid:15663921 doi:10.1007/s11892-005-0071-7 yong-ho lee richard e pratley arteriosclerosis / physiopathology diabetic angiopathies / physiopathology

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