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Sci Rep. 2019 Feb 12;9(1):1816. doi: 10.1038/s41598-018-37704-2.

Exposure to Nanoscale Particulate Matter from Gestation to Adulthood Impairs Metabolic Homeostasis in Mice.

Author information

1
Departments of Preventive Medicine and Biochemistry & Molecular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA.
2
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, California, 90089, USA.
3
The Saban Research Institute, Developmental Neuroscience Program and Diabetes and Obesity Program, Center for Endocrinology, Diabetes and Metabolism, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA, 90027, USA.
4
Inserm, Jean-Pierre Aubert Research Center, U1172, University Lille 2, Lille, 59045, France.
5
Department of Civil and Environmental Engineering, Viterbi School of Engineering, University of Southern California, Los Angeles, California, 90089, USA.
6
Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA.
7
Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, 90095, USA.
8
Department of Environmental Health Sciences, Fielding School of Public Health at UCLA, Los Angeles, CA, 90095, USA.
9
Departments of Preventive Medicine and Biochemistry & Molecular Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA. hallayee@usc.edu.

Abstract

Emerging evidence from epidemiological and animal studies suggests that exposure to traffic-related air pollutants and particulate matter less than 2.5 µm in diameter (PM2.5) contributes to development of obesity and related metabolic abnormalities. However, it is not known whether nanoscale particulate matter (nPM) with aerodynamic diameter ≤200 nm have similar adverse metabolic effects. The goal of the present study was to determine the effects of prenatal and early life exposure to nPM on metabolic homeostasis in mice. C57BL/6 J mice were exposed to nPM or filtered air from gestation until 17 weeks of age and characterized for metabolic and behavioral parameters. In male mice, nPM exposure increased food intake, body weight, fat mass, adiposity, and whole-body glucose intolerance (p < 0.05). Consistent with these effects, male mice exposed to nPM displayed alterations in the expression of metabolically-relevant neuropeptides in the hypothalamus and decreased expression of insulin receptor signaling genes in adipose (p < 0.05). There were no differences in exploratory behavior or motor function, fasting lipid levels, or the inflammatory profile of adipose tissue. Our results provide evidence that chronic nPM exposure from gestation to early adulthood in male mice promotes metabolic dysregulation in part through modulation of feeding behavior and in the absence of an obesogenic diet.

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