Journal Article

Long-term Exposure to Ambient Fine Particulate Pollution Induces Insulin Resistance and Mitochondrial Alteration in Adipose Tissue

Xiaohua Xu, Cuiqing Liu, Zhaobin Xu, Kevin Tzan, Mianhua Zhong, Aixia Wang, Morton Lippmann, Lung-Chi Chen, Sanjay Rajagopalan and Qinghua Sun

in Toxicological Sciences

Volume 124, issue 1, pages 88-98
Published in print November 2011 | ISSN: 1096-6080
Published online August 2011 | e-ISSN: 1096-0929 | DOI: http://dx.doi.org/10.1093/toxsci/kfr211
Long-term Exposure to Ambient Fine Particulate Pollution Induces Insulin Resistance and Mitochondrial Alteration in Adipose Tissue

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We have previously shown that chronic exposure to ambient fine particulate matter (less than 2.5 μm 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.

Keywords: air pollution; inflammation; glucose tolerance; mitochondria

Journal Article.  4848 words.  Illustrated.

Subjects: Medical Toxicology ; Toxicology (Non-medical)

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