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Programming of mouse obesity by maternal exposure to concentrated ambient fine particles.

ABSTRACT: Many diseases including obesity may originate through alterations in the early-life environment that interrupts fetal development. Increasing evidence has shown that exposure to ambient fine particles (PM2.5) is associated with abnormal fetal development. However, its long-term metabolic effects on offspring have not been systematically investigated.To determine if maternal exposure to PM2.5 programs offspring obesity, female C57Bl/6j mice were exposed to filtered air (FA) or concentrated ambient PM2.5 (CAP) during pre-conception, pregnancy, and lactation, and the developmental and metabolic responses of offspring were assessed. The growth trajectory of offspring revealed that maternal exposure to CAP significantly decreased offspring birth weight but increased body weight of adult male but not female offspring, and the latter was expressed as increased adiposity. These adult male offspring had increased food intake, but were sensitive to exogenous leptin. Their hypothalamic expression of Socs3 and Pomc, two target genes of leptin, was not changed, and the hypothalamic expression of NPY, an orexigenic peptide that is inhibited by leptin, was significantly increased. These decreases in central anorexigenic signaling were accompanied by reduced plasma leptin and its expression in adipose tissues, the primary source of circulating leptin. In contrast, maternal exposure did not significantly change any of these indexes in adult female offspring. Pyrosequencing demonstrated that the leptin promoter methylation of adipocytes was significantly increased in CAP-exposed male but not female offspring.Our data indicate that maternal exposure to ambient PM2.5 programs obesity in male offspring probably through alterations in the methylation of the promoter region of the leptin gene.

SUBMITTER: Chen M

PROVIDER: S-EPMC5481884 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature

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Programming of mouse obesity by maternal exposure to concentrated ambient fine particles.

Chen Minjie M Wang Xiaoke X Hu Ziying Z Zhou Huifen H Xu Yanyi Y Qiu Lianglin L Qin Xiaobo X Zhang Yuhao Y Ying Zhekang Z

Particle and fibre toxicology 20170623 1

<h4>Background</h4>Many diseases including obesity may originate through alterations in the early-life environment that interrupts fetal development. Increasing evidence has shown that exposure to ambient fine particles (PM<sub>2.5</sub>) is associated with abnormal fetal development. However, its long-term metabolic effects on offspring have not been systematically investigated.<h4>Results</h4>To determine if maternal exposure to PM<sub>2.5</sub> programs offspring obesity, female C57Bl/6j mice ...[more]

PMID: 28645299

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Project description:BackgroundRecent epidemiological studies indicate negative associations between a diverse group of air pollutants and cognitive functioning in children and adults, and aspects of attention deficit in children. Neuroinflammation and oxidative stress are two putative biological mechanisms by which air pollutants may adversely affect the brain.ObjectivesWe sought to determine whether exposure to concentrated ambient particulate matter (CAPS) during the first 2 weeks of life, alone or again in adulthood, could alter responding for delayed reward, a critical component of human decision making. Greater preference for immediate reward has been implicated as a component of several psychiatric disorders, addiction, obesity, and attention deficit.MethodsC57BL/6J mice were exposed to ultrafine particles (< 100 nm in aerodynamic diameter; CAPS) using the Harvard University Concentrated Ambient Particle System (HUCAPS) or filtered air in the postnatal period (days 4-7 and 10-13) with and without adult exposure over days 56-60. In adulthood, delay behavior was assessed using a fixed-ratio waiting-for-reward (FR wait) paradigm in which 25 responses (FR25) were required to initiate the waiting-for-reward component during which mice obtained "free" sucrose pellets with the stipulation that these "free" pellets were delivered at increasing delay intervals.ResultsCoupled with increased FR response rates, mice exposed to postnatal CAPS displayed increased FR resets that reinstated short delays, indicating a preference for shorter delays, despite the added response cost of the FR25. No associated changes in locomotor activity were observed.ConclusionsPostnatal CAPS exposure produces an enhanced bias towards immediate rewards, a risk factor for several central nervous system (CNS) disorders. This enhancement does not appear to be the result of hyperactivity. The findings underscore the need for further evaluation of air pollution effects on the CNS and its potential contribution to CNS diseases and disorders.

Project description:BackgroundFetal growth restriction (FGR) is not only a major determinant of perinatal morbidity and mortality but also leads to adverse health effects in later life. Over the past decade, numerous studies have indicated that maternal exposure to ambient air pollution has been a risk factor for abnormal fetal growth in developed countries where PM2.5 levels are relatively low. However, studies in highly polluted regions, such as China, and studies that rely on assessments in utero are scarce.MethodsA total of 7965 women were selected from 11,441 women from the Shanghai Maternity and Infant Living Environment (SMILE) cohort who were pregnant between January 1, 2014, and April 30, 2015. From January 1, 2014, to April 30, 2015, weekly average PM2.5 values from 53 monitors were calculated and the inverse distance weighted (IDW) method was used to create a Shanghai pollution surface map according to the participants residential addresses. Individual exposure was the average PM2.5 value of every gestational week between the first gestational week and one week before the ultrasound measurement date (the range of measurements per participant was 1 to 10). Repeated fetal ultrasound measurements during gestational weeks 14~40 were selected. The estimated fetal weight (EFW) was calculated by biparietal diameter (BPD), abdominal circumference (AC), and femur length (FL) formulas. In total, 29,926 ultrasound measurements were analysed. Demographic variables, other pollutants (SO2, NO2, PM10 and O3) and relative humidity and temperature were controlled for potential confounding through generalized estimating equations (GEE).ResultsThe full model showed that with each 10 μg/m3 increase in PM2.5 exposure, the means (mm) of AC, BPD, FL decreased by 5.48 (- 9.06, - 1.91), 5.57 (- 6.66, - 4.47), and 5.47 (- 6.39, - 4.55), respectively; the mean EFW decreased by 14.49 (- 16.05, - 13.49) grams by Hadlock's third formula and 13.56 (- 14.71, - 12.50) grams by Shepard's formula with each 10 μg/m3 increase in PM2.5 exposure.ConclusionsA negative correlation existed between maternal PM2.5 exposure during pregnancy and fetal growth indicators, which may increase the risk of fetal growth restriction.

Project description:BackgroundAlthough previous studies suggest that exposure to traffic-related pollution during childhood increases the risk of childhood overweight or obesity (COWO), the role of early life exposure to fine particulate matter (aerodynamic diameter <2.5 ?m; PM2.5) and its joint effect with the mother’s prepregnancy body mass index (MPBMI) on COWO remain unclear.ObjectivesThe present study was conducted to examine the individual and joint effects of ambient PM2.5 exposures and MPBMI on the risk of COWO.MethodsWe estimated exposures to ambient PM2.5in utero and during the first 2 y of life (F2YL), using data from the U.S. Environmental Protection Agency’s (EPA’s) Air Quality System matched to residential address, in 1,446 mother–infant pairs who were recruited at birth from 1998 and followed up prospectively through 2012 at the Boston Medical Center in Massachusetts. We quantified the individual and joint effects of PM2.5 exposure with MPBMI on COWO, defined as the child’s age- and sex-specific BMI z-score ?85th?percentile at the last well-child care visit between 2 and 9 y of age. Additivity was assessed by estimating the reduced excess risk due to interaction.ResultsComparing the highest and lowest quartiles of PM2.5, the adjusted relative risks (RRs) [95% confidence intervals (CIs)] of COWO were 1.3 (95% CI: 1.1, 1.5), 1.2 (95% CI: 1.0, 1.4), 1.2 (95% CI: 1.0, 1.4), 1.3 (95% CI: 1.1, 1.6), 1.3 (95% CI: 1.1, 1.5) and 1.3 (1.1, 1.5) during preconception; the first, second, and third trimesters; the entire period of pregnancy; and F2YL, respectively. Spline regression showed a dose–response relationship between PM2.5 levels and COWO after a threshold near the median exposure (10.46 ?g/m3–10.89 ?g/m3). Compared with their counterparts, children of obese mothers exposed to high levels of PM2.5 had the highest risk of COWO [RR?2.0, relative excess risk due to interaction (RERI) not significant].ConclusionsIn the present study, we observed that early life exposure to PM2.5 may play an important role in the early life origins of COWO and may increase the risk of COWO in children of mothers who were overweight or obese before pregnancy beyond the risk that can be attributed to MPBMI alone. Our findings emphasize the clinical and public health policy relevance of early life PM2.5 exposure. https://doi.org/10.1289/EHP261

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Programming of mouse obesity by maternal exposure to concentrated ambient fine particles.

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Programming of mouse obesity by maternal exposure to concentrated ambient fine particles.

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