State Key Laboratory of Environmental and Biological Analysis, Hong Kong Baptist University, Hong Kong, SAR, China.
State Key Laboratory of Environmental and Biological Analysis, Hong Kong Baptist University, Hong Kong, SAR, China; HKBU Institute for Research and Continuing Education, Shenzhen, China.
Sci Total Environ. 2019 Mar 20;657:1389-1397. doi: 10.1016/j.scitotenv.2018.12.007. Epub 2018 Dec 3.
Prenatal exposure to ambient fine particles (diameter < 0.25 μm, PM) has been found to be associated with abnormal growth and development in offspring. However, the effects of PM on the lipid metabolism of adipose tissue in offspring are unclear. In the present study, we established a mouse model of prenatal exposure to PM by intratracheal instillation to pregnant C57BL/6 female mice with PM suspension or normal saline. We found that prenatal exposure to PM of a mouse model reduced body weight in adult male offspring after 6 weeks old. Histological analysis showed that the adipocyte size was significantly reduced in epididymal adipose tissue (eWAT) in male offspring, but not in brown adipose tissue. The expression levels of genes related to fatty acid synthesis (ACC1, ACSL1) and oxidation (PPARα) in eWAT were also significantly decreased. In addition, downregulation of pro-inflammatory cytokines (TNFα, IL-1β, IL-6) was also observed. Lipidomics analysis of eWAT demonstrated that prenatal exposure of PM reduced lysophosphatidylcholines (LPC), phosphatidylcholines (PC), phosphatidylethanolamines (PE), sphingomyelins (SM), and ceramides (Cer), indicating that metabolic pathways, including SM-Cer signaling and glycerophospholipids remodeling, were disrupted. In summary, prenatal exposure to PM was associated with the dysregulations in lipid metabolism of eWAT and pro-inflammatory response in male offspring.
产前暴露于环境细颗粒物（直径<0.25μm，PM）已被发现与后代生长和发育异常有关。然而，PM 对后代脂肪组织脂质代谢的影响尚不清楚。在本研究中，我们通过气管内滴注 PM 悬浮液或生理盐水建立了 PM 暴露于孕鼠的小鼠模型。我们发现，PM 暴露于该模型后，雄性子代在 6 周龄后体重减轻。组织学分析表明，雄性子代附睾脂肪组织（eWAT）中的脂肪细胞大小明显减小，但棕色脂肪组织没有变化。eWAT 中与脂肪酸合成（ACC1、ACSL1）和氧化（PPARα）相关的基因表达水平也明显降低。此外，促炎细胞因子（TNFα、IL-1β、IL-6）的下调也观察到。eWAT 的脂质组学分析表明，PM 的产前暴露降低了溶血磷脂酰胆碱（LPC）、磷脂酰胆碱（PC）、磷脂酰乙醇胺（PE）、鞘磷脂（SM）和神经酰胺（Cer）的水平，表明包括 SM-Cer 信号和甘油磷脂重塑在内的代谢途径受到干扰。总之，产前 PM 暴露与雄性子代 eWAT 脂质代谢失调和促炎反应有关。
