Ⅱ型糖尿病在發(fā)達國家中的發(fā)生率正在上升之中。如今,，研究人員發(fā)現(xiàn),，一種新近鑒別出的蛋白質(zhì)可能在Ⅱ型糖尿病的發(fā)生過程中發(fā)揮了關(guān)鍵作用，新成果發(fā)表在12月在線出版的《自然—免疫學(xué)》期刊上,。也許,，以這種炎癥通道的組分為靶標，將引導(dǎo)Ⅱ型糖尿病新治療方法的研發(fā),。
以前的研究顯示,，一種名為TXNIP的蛋白質(zhì)與胰島素抗性有關(guān)。Jürg Tschopp和同事最近發(fā)現(xiàn),，TXNIP與炎癥因子NLRP3的啟動密切相關(guān),，NLRP3是一種負責(zé)調(diào)控免炎癥和疫信使因子IL-1beta生產(chǎn)的復(fù)合 蛋白質(zhì)。各種壓力和危險信號如感染等會促使TXNIP從休眠狀態(tài)進入活躍狀態(tài),，激活炎癥因子NLRP3并釋放出IL-1beta,。多糖癥是血液中糖分過量 的癥狀，多糖癥引誘基于TXNIP的IL-1beta以某種方式從細胞中釋放,，從而出現(xiàn)了在糖尿病患者中觀察到的慢性炎癥,。
新研究發(fā)現(xiàn)了多糖癥與炎癥間的一種關(guān)聯(lián)，如果科學(xué)家們發(fā)現(xiàn)了瞄準炎癥因子NLRP3組成的方法,，那么這將有利于指導(dǎo)Ⅱ型糖尿病和其他炎癥性疾病的新治療方法的研發(fā),。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
