期刊
TOXICOLOGICAL SCIENCES
卷 124, 期 1, 页码 88-98出版社
OXFORD UNIV PRESS
DOI: 10.1093/toxsci/kfr211
关键词
air pollution; inflammation; glucose tolerance; mitochondria
类别
资金
- National Institutes of Health [ES016588, ES017412, ES018900, ES015146, ES00260]
- Diabetes Action Research and Education Foundation
We have previously shown that chronic exposure to ambient fine particulate matter (less than 2.5 mu m in aerodynamic diameter, PM2.5) pollution in conjunction with high-fat diet induces insulin resistance through alterations in inflammatory pathways. In this study, we evaluated the effects of PM2.5 exposure over a substantive duration of a rodent's lifespan and focused on the impact of long-term exposure on adipose structure and function. C57BL/6 mice were exposed to PM2.5 or filtered air (FA) (6 h/day, 5 days/week) for duration of 10 months in Columbus, OH. At the end of the exposure, PM2.5-exposed mice demonstrated insulin resistance (IR) and a decrease in glucose tolerance compared with the FA-exposed group. Although there were no significant differences in circulating cytokines between PM2.5- and FA-exposed groups, circulating adiponectin and leptin were significantly decreased in PM2.5-exposed group. PM2.5 exposure also led to inflammatory response and oxidative stress as evidenced by increase of Nrf2-regulated antioxidant genes. Additionally, PM2.5 exposure decreased mitochondrial count in visceral adipose and mitochondrial size in interscapular adipose depots, which were associated with reduction of uncoupling protein 1 (UCP1) expression and downregulation of brown adipocyte-specific gene profiles. These findings suggest that long-term ambient PM2.5 exposure induces impaired glucose tolerance, IR, inflammation, and mitochondrial alteration, and thus, it is a risk factor for the development of type 2 diabetes.
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