Timing determines programming of energy homeostasis by maternal PM 2.5 exposure in mouse models.

Autor: Wang S; Department of Medicine Cardiology Division, University of Maryland School of Medicine, Baltimore, MD, 21201, USA., Peng R; Department of Environmental Health, School of Public Health, Fudan University, Shanghai, 200032, China., Chen H; Department of Medicine Cardiology Division, University of Maryland School of Medicine, Baltimore, MD, 21201, USA., Han D; Department of Environmental Health, School of Public Health, Fudan University, Shanghai, 200032, China., Wu J; Department of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, MD, 21201, USA., Xu Y; Department of Environmental Health, School of Public Health, Fudan University, Shanghai, 200032, China. Electronic address: yanyi_xu@fudan.edu.cn., Ying Z; Department of Medicine Cardiology Division, University of Maryland School of Medicine, Baltimore, MD, 21201, USA. Electronic address: zying@medicine.umaryland.edu.
Jazyk: angličtina
Zdroj: Environmental pollution (Barking, Essex : 1987) [Environ Pollut] 2024 Dec 15; Vol. 363 (Pt 2), pp. 125187. Date of Electronic Publication: 2024 Oct 23.
DOI: 10.1016/j.envpol.2024.125187
Abstrakt: Maternal exposure to particulate matter with an aerodynamic diameter ≤2.5 μm (PM 2.5 ) is believed to be a risk factor of developmental origins of health and disease (DOHaD), but its effect on offspring's susceptibility to obesity, a common target disease of DOHaD, remains controversial. To pinpoint the effect of maternal PM 2.5 exposure on offspring's energy homeostasis, female C57BL/6J mice were exposed to filtered air (FA) or concentrated ambient PM 2.5 (CAP) for 12 weeks and mated with normal male mice to produce offspring. After parturition, a cross-fostering strategy was exploited to determine whether prenatal and/or postnatal mothering by CAP-exposed dams program offspring's energy homeostasis and susceptibility to obesity. Moreover, oocytes were collected from FA- or CAP-exposed mice and subjected to in vitro fertilization (IVF) to determine whether maternal pre-conceptional exposure to PM 2.5 programs energy homeostasis. Results showed that prenatal mothering by CAP-exposed dams increased suckling's milk intake and weight gain, decreased normal diet (ND)-fed offspring's adulthood food intake and body weight, and did not influence offspring's diet-induced obesity (DIO). Postnatal mothering by CAP-exposed dams did not influence suckling's milk intake and weight gain, increased ND-fed offspring's adulthood food intake and body weight and did not influence offspring's DIO. Prenatal plus postnatal mothering by CAP-exposed dams increased suckling's milk intake and weight gain, increased ND-fed offspring's adulthood food intake and body weight, and aggravated offspring's DIO. IVF study revealed that male offspring derived from CAP-exposed mice versus controls had significantly decreased adulthood food intake and body weight. RNA sequencing showed that CAP exposure influenced oocyte estrogen signaling and histone methylation. This study thus clearly reveals that timing determines programming of energy homeostasis by maternal PM 2.5 exposure.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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