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首页> 外文期刊>Journal of applied toxicology >Maternal organophosphate flame-retardant exposure alters offspring energy and glucose homeostasis in a sexually dimorphic manner in mice
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Maternal organophosphate flame-retardant exposure alters offspring energy and glucose homeostasis in a sexually dimorphic manner in mice

机译：母体有机磷酸盐阻燃暴露在小鼠中改变后代能量和葡萄糖稳态

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摘要

Persistent organic pollutants such as organophosphate flame retardants (OPFRs) can accumulate in the body and interact with nuclear receptors that control energy homeostasis. One sensitive window of exposure is during development, either in utero or neonatal. Therefore, we investigated if maternal exposure to a mixture of OPFRs alters metabolism on a low-fat diet (LFD) or a high-fat diet (HFD) in both male and female offspring. Wild-type C57Bl/6J dams were orally dosed with vehicle (sesame oil) or an OPFR mixture (1 mg/kg each of tris(1,3-dichloro-2-propyl)phosphate, triphenyl phosphate, and tricresyl phosphate) from gestation day 7 to postnatal day 14. After weaning, pups were fed LFD or HFD. To assess metabolism, we measured body weight and food intake weekly and determined body composition, metabolism, activity, and glucose homeostasis at 6 months of age. Although maternal OPFR exposure did not alter body weight or adiposity, OPFR exposure altered substrate utilization and energy expenditure depending on diet in both sexes. Systolic and diastolic blood pressure was increased by OPFR in male offspring. OPFR exposure interacted with HFD to increase fasting glucose in females and alter glucose and insulin tolerance in male offspring. Plasma leptin was reduced in male and female offspring when fed HFD, whereas liver expression ofPepck was increased in femalesandEsr1(estrogen receptor alpha) was increased in both sex. The physiological implications indicate maternal exposure to OPFRs programs peripheral organs including the liver and adipose tissue, in a sex-dependent manner, thus changing the response to an obesogenic diet and altering adult offspring energy homeostasis.
机译：持久性有机污染物，如有机磷阻燃剂（OPFRs），可在体内积聚，并与控制能量稳态的核受体相互作用。一个敏感的暴露窗口是在发育过程中，无论是在子宫内还是新生儿。因此，我们调查了母亲接触OPFRs混合物是否会改变男性和女性后代在低脂饮食（LFD）或高脂饮食（HFD）中的代谢。从妊娠第7天到产后第14天，野生型C57Bl/6J母鼠口服赋形剂（芝麻油）或OPFR混合物（磷酸三（1,3-二氯-2-丙基）、磷酸三苯酯和磷酸三甲酚酯各1 mg/kg）。断奶后，给幼崽喂食LFD或HFD。为了评估代谢，我们每周测量体重和食物摄入量，并在6个月大时测定身体成分、代谢、活动和葡萄糖稳态。尽管母体OPFR暴露不会改变体重或肥胖，但OPFR暴露会改变底物利用率和能量消耗，这取决于两性的饮食。OPFR使雄性后代的收缩压和舒张压升高。OPFR暴露与HFD相互作用，增加女性的空腹血糖，并改变男性后代的葡萄糖和胰岛素耐受性。喂食HFD后，雄性和雌性后代的血浆瘦素水平降低，而雌性后代的肝脏EPCK表达增加，雌性和雌性后代的雌激素受体α1水平均升高。生理学意义表明，母亲以性别依赖的方式接触OPFRs会影响包括肝脏和脂肪组织在内的外周器官，从而改变对肥胖饮食的反应，并改变成年后代的能量平衡。

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