The evolving role of inflammation in obesity and the metabolic syndrome

被引：17

作者：

Lee Y.-H. ^{[1
]}

Pratley R.E. ^{[1
]}

机构：

[1] Diabet./Metabolism Transl. Med. Unit, Division of Endocrinology/Metabolism, Univ. of Vermont College of Medicine, Burlington, VT 05401, One South Prospect Street

来源：

Current Diabetes Reports | 2005年 / 5卷 / 1期

关键词：

Obesity; Insulin Resistance; Adipose Tissue; Metabolic Syndrome; Insulin Action;

D O I：

10.1007/s11892-005-0071-7

中图分类号：

学科分类号：

摘要：

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-ractive protein, are increased in obesity, associated with insullin 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 treatmant and prevention strategies aimed at reducing obesity-associated morbidities and mortality. Copyright © 2005 by Current Science Inc.

引用

页码：70 / 75

页数：5

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