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DOI | 10.1289/EHP4591 |
Glucose Homeostasis following Diesel Exhaust Particulate Matter Exposure in a Lung Epithelial Cell-Specific IKK2-Deficient Mouse Model | |
Chen, Sufang1,2; Chen, Minjie2; Wei, Wei2,3; Qiu, Lianglin2,4; Zhang, Li2; Cao, Qi5; Ying, Zhekang2 | |
2019-05-01 | |
发表期刊 | ENVIRONMENTAL HEALTH PERSPECTIVES |
ISSN | 0091-6765 |
EISSN | 1552-9924 |
出版年 | 2019 |
卷号 | 127期号:5 |
文章类型 | Article |
语种 | 英语 |
国家 | Peoples R China; USA |
英文摘要 | Background: Pulmonary inflammation is believed to be central to the pathogenesis due to exposure to fine particulate matter with aerodynamic diameter <= 2.5 mu m (PM2.5). This central role, however, has not yet been systemically examined. Objective: In the present study, we exploited a lung epithelial cell-specific inhibitor kappa B kinase 2 (IKK2) knockout mouse model to determine the role of pulmonary inflammation in the pathophysiology due to exposure to diesel exhaust particulate matter (DEP). Methods: SFTPC-rtTA(+/-)tetO-cre(+/-)IKK2(flox/flox) (lung epithelial cell-specific IKK2 knockout, KO) and SFTPC-rtTA(+/-)tetO-cre(+/-)IKK2(flox/flox) (wild-type, tgWT) mice were intratracheally instilled with either vehicle or DEP for 4 months, and their inflammatory response and glucose homeostasis were then assessed. Results: In comparison with tgWT mice, lung epithelial cell-specific IKK2-deficient mice had fewer DEP exposure-induced bronchoalveolar lavage fluid immune cells and proinflammatory cytokines as well as fewer DEP exposure-induced circulating proinflammatory cytokines. Glucose and insulin tolerance tests revealed that lung epithelial cell-specific IKK2 deficiency resulted in markedly less DEP exposure-induced insulin resistance and greater glucose tolerance. Akt phosphorylation analyses of insulin-responsive tissues showed that DEP exposure primarily targeted hepatic insulin sensitivity. Lung epithelial cell-specific IKK2-deficient mice had significantly lower hepatic insulin resistance than tgWT mice had. Furthermore, this difference in insulin resistance was accompanied by consistent differences in hepatic insulin receptor substrate 1 serine phosphorylation and inflammatory marker expression. Discussion: Our findings suggest that in a tissue-specific knockout mouse model, an IKK2-dependent pulmonary inflammatory response was essential for the development of abnormal glucose homeostasis due to exposure to DEP. |
领域 | 资源环境 |
收录类别 | SCI-E |
WOS记录号 | WOS:000471116100012 |
WOS关键词 | KAPPA-B ACTIVATION ; AIR-POLLUTION ; INFLAMMATORY RESPONSES ; CARDIOVASCULAR-DISEASE ; INSULIN SENSITIVITY ; IKK-BETA ; PARTICLE ; INSTILLATION ; TARGET ; MICE |
WOS类目 | Environmental Sciences ; Public, Environmental & Occupational Health ; Toxicology |
WOS研究方向 | Environmental Sciences & Ecology ; Public, Environmental & Occupational Health ; Toxicology |
引用统计 | |
文献类型 | 期刊论文 |
条目标识符 | http://119.78.100.173/C666/handle/2XK7JSWQ/182809 |
专题 | 资源环境科学 |
作者单位 | 1.Zhengzhou Univ, Affiliated Hosp 1, Dept Geriatr Endocrinol, Zhengzhou, Henan, Peoples R China; 2.Univ Maryland, Sch Med, Dept Med, Cardiol Div, Baltimore, MD 21201 USA; 3.Cent S Univ, Xiangya Hosp, Dept Bile Pancreat Surg, Changsha, Hunan, Peoples R China; 4.Nantong Univ, Sch Publ Hlth, Dept Occupat & Environm Hlth, Nantong, Peoples R China; 5.Univ Maryland, Sch Med, Dept Diagnost Radiol & Nucl Med, Baltimore, MD 21201 USA |
推荐引用方式 GB/T 7714 | Chen, Sufang,Chen, Minjie,Wei, Wei,et al. Glucose Homeostasis following Diesel Exhaust Particulate Matter Exposure in a Lung Epithelial Cell-Specific IKK2-Deficient Mouse Model[J]. ENVIRONMENTAL HEALTH PERSPECTIVES,2019,127(5). |
APA | Chen, Sufang.,Chen, Minjie.,Wei, Wei.,Qiu, Lianglin.,Zhang, Li.,...&Ying, Zhekang.(2019).Glucose Homeostasis following Diesel Exhaust Particulate Matter Exposure in a Lung Epithelial Cell-Specific IKK2-Deficient Mouse Model.ENVIRONMENTAL HEALTH PERSPECTIVES,127(5). |
MLA | Chen, Sufang,et al."Glucose Homeostasis following Diesel Exhaust Particulate Matter Exposure in a Lung Epithelial Cell-Specific IKK2-Deficient Mouse Model".ENVIRONMENTAL HEALTH PERSPECTIVES 127.5(2019). |
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