Epidemiological and experimental links between air pollution and type 2 diabetes.
Epidemiological and experimental links between air pollution and type 2 diabetes.
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DOI：
10.1177/0192623312464531
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发表时间：
2013-02
影响因子：
1.5
通讯作者：
Rajagopalan S
中科院分区：
文献类型：
--
作者：
Liu C;Ying Z;Harkema J;Sun Q;Rajagopalan S
越来越多的证据表明，暴露于环境毒素和2型糖尿病（DM）的易感性之间的联系。在这篇综述中，我们总结了实验证据，以支持这种协会已指出，在许多流行病学研究。空气污染中颗粒物（PM2.5）暴露引起的炎症反应是一种常见的机制，可能与饮食和生活方式中的其他促炎影响相互作用，以调节对心脏代谢疾病的易感性。从肺中的巨噬细胞释放的先天免疫细胞因子的作用是众所周知的。此外，响应于空气污染暴露的趋化因子触发物可以通过Toll样受体（TLR）和核苷酸寡聚化结构域受体（NLR）途径介导来自骨髓/脾脏的细胞应答，以介导器官中的炎症应答。新出现的数据似乎也支持PM2.5暴露在内质网应激诱导的细胞凋亡和棕色脂肪组织功能障碍中的作用。棕色脂肪组织中UCP 1表达的减少可能是产热减少的原因，这提供了PM2.5和胰岛素抵抗之间的另一种联系。空气污染暴露和2型糖尿病之间的实验联系的影响是深远的，因为空气污染是一个普遍的风险因素，在世界各地，即使是轻微的缓解暴露可能会提供大量的公共健康利益。
There is increasing evidence suggesting links between exposure to environmental toxins and susceptibility to type 2 diabetes mellitus (DM). In this review we summarize the experimental evidence to support this association which has been noted in many epidemiologic studies. Inflammation in response to particulate matter (PM2.5) exposure in air-pollution represents a common mechanism that may interact with other pro-inflammatory influences in diet and life style to modulate susceptibility to cardiometabolic diseases. The role of innate immune cytokines released from macrophages in the lung is well known. In addition, chemokine triggers in response to air-pollution exposure may mediate a cellular response from the bone marrow/spleen through toll-like receptors (TLRs) and Nucleotide Oligomerization Domain receptors (NLRs) pathways to mediate inflammatory response in organs. Emerging data also seems to support a role for PM2.5 exposure in endoplasmic reticulum stress-induced apoptosis and in brown adipose tissue dysfunction. Decreased expression of UCP1 in brown adipose tissue may account for reduced thermogenesis providing another link between PM2.5 and insulin resistance. The implications of an experimental link between air-pollution exposure and type 2 DM are profound as air-pollution is a pervasive risk factor throughout the world and even modest alleviation in exposure may provide substantial public health benefits.
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影响因子：
16.2
作者：
Andersen ZJ;Raaschou-Nielsen O;Ketzel M;Jensen SS;Hvidberg M;Loft S;Tjønneland A;Overvad K;Sørensen M
通讯作者：
Sørensen M
DOI：
10.1165/ajrcmb.27.1.4787
发表时间：
2002-07-01
影响因子：
6.4
作者：
Fujii, T;Hayashi, S;van Eeden, SF
通讯作者：
van Eeden, SF
影响因子：
15.9
作者：
Block, Michelle L.;Calderon-Garciduenas, Lilian
通讯作者：
Calderon-Garciduenas, Lilian
影响因子：
10.4
作者：
Frampton MW;Stewart JC;Oberdörster G;Morrow PE;Chalupa D;Pietropaoli AP;Frasier LM;Speers DM;Cox C;Huang LS;Utell MJ
通讯作者：
Utell MJ
影响因子：
2.1
作者：
Ghio, AJ;Hall, A;Devlin, RB
通讯作者：
Devlin, RB