Abstract
We have investigated the effects of in utero exposure to environmentally persistent free radicals (EPFRs) on growth, metabolism, energy utilization, and skeletal muscle mitochondria in a mouse model of diet-induced obesity. Pregnant mice were treated with laboratory-generated, combustion-derived particular matter (MCP230). The adult offspring were placed on a high-fat diet for 12 wk, after which we observed a 9.8% increase in their body weight. The increase in body size observed in the MCP230-exposed mice was not associated with increases in food intake but was associated with a reduction in physical activity and lower energy expenditure. The reduced energy expenditure in mice indirectly exposed to MCP230 was associated with reductions in skeletal muscle mitochondrial DNA copy number, lower mRNA levels of electron transport genes, and reduced citrate synthase activity. Upregulation of key genes involved in ameliorating oxidative stress was also observed in the muscle of MCP230-exposed mice. These findings suggest that gestational exposure to MCP230 leads to a reduction in energy expenditure at least in part through alterations to mitochondrial metabolism in the skeletal muscle.
Highlights
OBESITY IS A MAJOR GLOBAL HEALTH CONCERN, and emerging data support a role for environmental pollutants in the pathogenesis of obesity and its comorbidities [2, 7, 9, 10, 12, 22, 24, 45]
We tested some of the metabolic effects of a limited gestational exposure to a recently realized environmental pollutant that is present in most combustion-derived particulate matter (PM): environmentally persistent free radicals (EPFRs)
Each exposure of MCP230 that the mothers received was the equivalent to a human breathing 200 g/m3 of EPFR, which is similar to what would be inhaled on a typical day in one of the major US cities [38]
Summary
OBESITY IS A MAJOR GLOBAL HEALTH CONCERN, and emerging data support a role for environmental pollutants in the pathogenesis of obesity and its comorbidities [2, 7, 9, 10, 12, 22, 24, 45]. Gestational and early-life exposure to combustion-derived particulate matter (PM) has been associated with an increased risk of obesity in humans [9, 12, 18, 22, 24]. This association is supported by data obtained from animal studies, where the offspring of pregnant mice, which have been exposed to diesel exhaust in utero, are predisposed to weight gain as adults [6]. We investigated the effects of in utero exposure to EPFRs on growth, metabolism, energy utilization, and skeletal muscle mitochondria in a mouse model of diet-induced obesity. We hypothesized that gestational exposure to EPFRs reduces energy expenditure and results in mitochondrial impairments in the skeletal muscle
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