Increased systemic and adipose tissue inflammation differentiates obese women with T2DM from obese women with normal glucose tolerance

Increased systemic and adipose tissue inflammation differentiates obese women with T2DM from... 1 Introduction</h5> The metabolic syndrome comprises a combination of risk factors that increase the risk of developing type-2 diabetes and cardiovascular disease [1] . Obesity, in particular abdominal obesity, is one of the main risk factors of the metabolic syndrome. The majority of obese individuals (~ 80%) will eventually develop metabolic abnormalities associated with a reduced life expectancy. However, there is a subset of obese individuals who remain relatively insulin sensitive and metabolically healthy throughout life [2] . The reason why these individuals are unaffected is still not completely understood.</P>The pathological metabolic consequences of obesity are closely linked to the expanding adipose tissue that at a certain level responds with stress signals to the energy overload [3] . Adipose tissue functions as a metabolic and endocrine organ releasing fatty acids and adipokines, both of which have immune modulatory activities as reviewed in Refs. [4,5] . Obesity induces adipose tissue dysfunction with increased secretion of pro-inflammatory cytokines and chemokines. Adipose tissue acquires a chronic inflammatory state which is characterized by macrophage accumulation in crown like structures that surround stressed and dying adipocytes [6,7] . Adipose tissue inflammation may affect systemic immune responses that contribute to the initiation and progression http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Metabolism Elsevier

Increased systemic and adipose tissue inflammation differentiates obese women with T2DM from obese women with normal glucose tolerance

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Publisher
Elsevier
Copyright
Copyright © 2014 Elsevier Inc.
ISSN
0026-0495
DOI
10.1016/j.metabol.2013.12.002
pmid
24467914
Publisher site
See Article on Publisher Site

Abstract

1 Introduction</h5> The metabolic syndrome comprises a combination of risk factors that increase the risk of developing type-2 diabetes and cardiovascular disease [1] . Obesity, in particular abdominal obesity, is one of the main risk factors of the metabolic syndrome. The majority of obese individuals (~ 80%) will eventually develop metabolic abnormalities associated with a reduced life expectancy. However, there is a subset of obese individuals who remain relatively insulin sensitive and metabolically healthy throughout life [2] . The reason why these individuals are unaffected is still not completely understood.</P>The pathological metabolic consequences of obesity are closely linked to the expanding adipose tissue that at a certain level responds with stress signals to the energy overload [3] . Adipose tissue functions as a metabolic and endocrine organ releasing fatty acids and adipokines, both of which have immune modulatory activities as reviewed in Refs. [4,5] . Obesity induces adipose tissue dysfunction with increased secretion of pro-inflammatory cytokines and chemokines. Adipose tissue acquires a chronic inflammatory state which is characterized by macrophage accumulation in crown like structures that surround stressed and dying adipocytes [6,7] . Adipose tissue inflammation may affect systemic immune responses that contribute to the initiation and progression

Journal

MetabolismElsevier

Published: Apr 1, 2014

References

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