![]() While the mechanisms for these adverse effects are not entirely known, these studies collectively suggest that ambient air pollution exposure impairs metabolic homeostasis through alterations of biological processes in the periphery as well as the central nervous system. Furthermore, in utero exposure to diesel exhaust particles (DEP), another model of TRAP, increased fetal brain inflammatory cytokines and, in conjunction with a high fat diet, led to microglial activation and increased anxiety in adulthood 23. These studies have shown that exposure to PM 2.5 modulates adiposity, particularly with respect to visceral fat accumulation, the development of glucose intolerance and other related metabolic abnormalities 20, 21, 22. For the most part, mouse studies focused on obesity have evaluated the effects of regional fine particulate matter, defined less than 2.5 µm in diameter (PM 2.5), with or without high fat feeding. The epidemiological data linking TRAP and obesity in humans has garnered considerable interest in the use of animal models to identify potential underlying pathophysiological mechanisms 18, 19. Collectively, these observations suggest that exposure to ambient air pollution, including during critical periods of development, may contribute to obesity in early life and its metabolic consequences later in adulthood. In adults, similar associations have been reported with higher incidence of metabolic syndrome, insulin resistance, and diabetes 9, 10, 11, 12, 13, 14, 15, 16, 17. For example, epidemiological studies have shown that prenatal and childhood exposure to ambient or traffic-related air pollutants (TRAP) is associated with more rapid BMI increases during childhood, increased prevalence of obesity, and metabolic dysregulation 2, 3, 4, 5, 6, 7, 8. However, emerging data from human and animal studies suggest that exposure to air pollution during in utero, early life, and later developmental periods may also play a role in the development of obesity and related metabolic abnormalities 1. In this regard, prior studies have focused on the imbalance between caloric intake and energy expenditure as one root environmental cause for the increased prevalence of obesity. It is generally accepted that obesity is characterized by lifetime exposure to an obesogenic environment in the context of genetic susceptibility factors. ![]() 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. There were no differences in exploratory behavior or motor function, fasting lipid levels, or the inflammatory profile of adipose tissue. 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). ![]() In male mice, nPM exposure increased food intake, body weight, fat mass, adiposity, and whole-body glucose intolerance (p < 0.05). 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. The goal of the present study was to determine the effects of prenatal and early life exposure to nPM on metabolic homeostasis in mice. ![]() However, it is not known whether nanoscale particulate matter (nPM) with aerodynamic diameter ≤200 nm have similar adverse metabolic effects. 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 (PM 2.5) contributes to development of obesity and related metabolic abnormalities.
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