Inflammation: the link between insulin resistance, obesity and diabetes

被引:1620
|
作者
Dandona, P
Aljada, A
Bandyopadhyay, A
机构
[1] SUNY Coll Buffalo, Div Endocrinol Diabet & Metab, Buffalo, NY 14209 USA
[2] Kaleida Hlth, Buffalo, NY 14209 USA
关键词
D O I
10.1016/j.it.2003.10.013
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interieukin-6 (IL-6), is increased in the insulin resistant states of obesity and type 2 diabetes, raising questions about the mechanisms underlying inflammation in these two conditions. It is also intriguing that an increase in inflammatory mediators or indices predicts the future development of obesity and diabetes. Two mechanisms might be involved in the pathogenesis of inflammation. Firstly, glucose and macronutrient intake causes oxidative stress and inflammatory changes. Chronic overnutrition (obesity) might thus be a proinflammatory state with oxidative stress. Secondly, the increased concentrations of TNF-alpha and IL-6, associated with obesity and type 2 diabetes, might interfere with insulin action by suppressing insulin signal transduction. This might interfere with the anti-inflammatory effect of insulin, which in turn might promote inflammation.
引用
收藏
页码:4 / 7
页数:4
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