胰岛素抵抗
炎症
促炎细胞因子
营养过剩
糖尿病
医学
内科学
内分泌学
氧化应激
胰岛素
2型糖尿病
发病机制
肥胖
肿瘤坏死因子α
免疫学
作者
Paresh Dandona,Ahmad Aljada,Arindam Bandyopadhyay
标识
DOI:10.1016/j.it.2003.10.013
摘要
Recent data have revealed that the plasma concentration of inflammatory mediators, such as tumour necrosis factor-alpha (TNF-alpha) and interleukin-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.
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