Prenatal exposure to ambient fine particles (diameter < 0.25 μm, PM2.5) has been found to be associated with abnormal growth and development in offspring. However, the effects of PM2.5 on the lipid metabolism of adipose tissue in offspring are unclear. In the present study, we established a mouse model of prenatal exposure to PM2.5 by intratracheal instillation to pregnant C57BL/6 female mice with PM2.5 suspension or normal saline. We found that prenatal exposure to PM2.5 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 PM2.5 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 PM2.5 was associated with the dysregulations in lipid metabolism of eWAT and pro-inflammatory response in male offspring.
Keywords: Adipocyte size; Ambient fine particles; Gestational exposure; Inflammatory response; Lipid metabolism.
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