Ⅱ型糖尿病在发达国家中的发生率正在上升之中。如今，研究人员发现，一种新近鉴别出的蛋白质可能在Ⅱ型糖尿病的发生过程中发挥了关键作用，新成果发表在12月在线出版的《自然—免疫学》期刊上。也许，以这种炎症通道的组分为靶标，将引导Ⅱ型糖尿病新治疗方法的研发。
以前的研究显示，一种名为TXNIP的蛋白质与胰岛素抗性有关。Jürg Tschopp和同事最近发现，TXNIP与炎症因子NLRP3的启动密切相关，NLRP3是一种负责调控免炎症和疫信使因子IL-1beta生产的复合 蛋白质。各种压力和危险信号如感染等会促使TXNIP从休眠状态进入活跃状态，激活炎症因子NLRP3并释放出IL-1beta。多糖症是血液中糖分过量 的症状，多糖症引诱基于TXNIP的IL-1beta以某种方式从细胞中释放，从而出现了在糖尿病患者中观察到的慢性炎症。
新研究发现了多糖症与炎症间的一种关联，如果科学家们发现了瞄准炎症因子NLRP3组成的方法，那么这将有利于指导Ⅱ型糖尿病和其他炎症性疾病的新治疗方法的研发。（生物谷Bioon.com）
生物谷推荐原始出处：
Nature Immunology 20 December 2009 | doi:10.1038/ni.1831
Thioredoxin-interacting protein links oxidative stress to inflammasome activation
Rongbin Zhou1, Aubry Tardivel1, Bernard Thorens2, Inpyo Choi3 & Jürg Tschopp1
The NLRP3 inflammasome has a major role in regulating innate immunity. Deregulated inflammasome activity is associated with several inflammatory diseases, yet little is known about the signaling pathways that lead to its activation. Here we show that NLRP3 interacted with thioredoxin (TRX)-interacting protein (TXNIP), a protein linked to insulin resistance. Inflammasome activators such as uric acid crystals induced the dissociation of TXNIP from thioredoxin in a reactive oxygen species (ROS)-sensitive manner and allowed it to bind NLRP3. TXNIP deficiency impaired activation of the NLRP3 inflammasome and subsequent secretion of interleukin 1β (IL-1β). Akin to Txnip?/? mice, Nlrp3?/? mice showed improved glucose tolerance and insulin sensitivity. The participation of TXNIP in the NLRP3 inflammasome activation may provide a mechanistic link to the observed involvement of IL-1β in the pathogenesis of type 2 diabetes.
1 Department of Biochemistry, University of Lausanne, Epalinges, Switzerland.
2 Center of Integrative Genomics, University of Lausanne, Epalinges, Switzerland.
3 Korea Research Institute of Bioscience and Biotechnology, Yusong, Taejon, Republic of Korea.
