Programming of mouse obesity by maternal exposure to concentrated ambient fine particles
Abstract Background 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 m...
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| Format: | Article |
| Language: | English |
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BMC
2017-06-01
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| Series: | Particle and Fibre Toxicology |
| Subjects: | |
| Online Access: | http://link.springer.com/article/10.1186/s12989-017-0201-9 |
| _version_ | 1811317690582695936 |
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| author | Minjie Chen Xiaoke Wang Ziying Hu Huifen Zhou Yanyi Xu Lianglin Qiu Xiaobo Qin Yuhao Zhang Zhekang Ying |
| author_facet | Minjie Chen Xiaoke Wang Ziying Hu Huifen Zhou Yanyi Xu Lianglin Qiu Xiaobo Qin Yuhao Zhang Zhekang Ying |
| author_sort | Minjie Chen |
| collection | DOAJ |
| description | Abstract Background 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. Results 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. Conclusions 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. |
| first_indexed | 2024-04-13T12:12:43Z |
| format | Article |
| id | doaj.art-6003fcfd1e0d44a28632cfdb468993ce |
| institution | Directory Open Access Journal |
| issn | 1743-8977 |
| language | English |
| last_indexed | 2024-04-13T12:12:43Z |
| publishDate | 2017-06-01 |
| publisher | BMC |
| record_format | Article |
| series | Particle and Fibre Toxicology |
| spelling | doaj.art-6003fcfd1e0d44a28632cfdb468993ce2022-12-22T02:47:27ZengBMCParticle and Fibre Toxicology1743-89772017-06-0114111310.1186/s12989-017-0201-9Programming of mouse obesity by maternal exposure to concentrated ambient fine particlesMinjie Chen0Xiaoke Wang1Ziying Hu2Huifen Zhou3Yanyi Xu4Lianglin Qiu5Xiaobo Qin6Yuhao Zhang7Zhekang Ying8Department of Environmental Health, School of Public Health, Fudan UniversityDepartment of Medicine Cardiology Division, University of Maryland School of MedicineDepartment of Medicine Cardiology Division, University of Maryland School of MedicineDepartment of Medicine Cardiology Division, University of Maryland School of MedicineDepartment of Environmental Health, School of Public Health, Fudan UniversityDepartment of Medicine Cardiology Division, University of Maryland School of MedicineDepartment of Medicine Cardiology Division, University of Maryland School of MedicineDepartment of Neurology, Zhongshan Hospital, Fudan UniversityDepartment of Environmental Health, School of Public Health, Fudan UniversityAbstract Background 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. Results 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. Conclusions 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.http://link.springer.com/article/10.1186/s12989-017-0201-9ObesityMaternal exposure to PM2.5Developmental programingLeptinDNA methylation |
| spellingShingle | Minjie Chen Xiaoke Wang Ziying Hu Huifen Zhou Yanyi Xu Lianglin Qiu Xiaobo Qin Yuhao Zhang Zhekang Ying Programming of mouse obesity by maternal exposure to concentrated ambient fine particles Particle and Fibre Toxicology Obesity Maternal exposure to PM2.5 Developmental programing Leptin DNA methylation |
| title | Programming of mouse obesity by maternal exposure to concentrated ambient fine particles |
| title_full | Programming of mouse obesity by maternal exposure to concentrated ambient fine particles |
| title_fullStr | Programming of mouse obesity by maternal exposure to concentrated ambient fine particles |
| title_full_unstemmed | Programming of mouse obesity by maternal exposure to concentrated ambient fine particles |
| title_short | Programming of mouse obesity by maternal exposure to concentrated ambient fine particles |
| title_sort | programming of mouse obesity by maternal exposure to concentrated ambient fine particles |
| topic | Obesity Maternal exposure to PM2.5 Developmental programing Leptin DNA methylation |
| url | http://link.springer.com/article/10.1186/s12989-017-0201-9 |
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