Dandona Paresh, Aljada Ahmad, Bandyopadhyay Arindam
Division of Endocrinology, Diabetes and Metabolism, State University of New York at Buffalo and Kaleida Health, 3 Gates Circle, Buffalo, NY 14209, USA.
Trends Immunol. 2004 Jan;25(1):4-7. doi: 10.1016/j.it.2003.10.013.
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.
最近的数据显示，在肥胖和2型糖尿病的胰岛素抵抗状态下，炎症介质如肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）的血浆浓度会升高，这引发了人们对这两种病症中炎症潜在机制的疑问。同样有趣的是，炎症介质或指标的升高预示着肥胖和糖尿病的未来发展。炎症的发病机制可能涉及两种机制。首先，葡萄糖和大量营养素的摄入会导致氧化应激和炎症变化。因此，慢性营养过剩（肥胖）可能是一种伴有氧化应激的促炎状态。其次，与肥胖和2型糖尿病相关的TNF-α和IL-6浓度升高，可能通过抑制胰岛素信号转导来干扰胰岛素作用。这可能会干扰胰岛素的抗炎作用，进而可能促进炎症。
