TY - JOUR
T1 - Prenatal exposure to ambient fine particulate matter induces dysregulations of lipid metabolism in adipose tissue in male offspring
AU - Xie, Peisi
AU - Zhao, Chao
AU - Huang, Wei
AU - Yong, Ting
AU - CHUNG, Chi Kong Arthur
AU - He, Kaiwu
AU - Chen, Xiangfeng
AU - CAI, Zongwei
N1 - Funding Information:
This work was supported by the National Natural Science Foundation of China (Grant No. 91543202 , 21507106 and 21806135 ) and the Collaborative Research Fund (Grant No. C2014-14E ) from Research Grants Council of Hong Kong.
PY - 2019/3/20
Y1 - 2019/3/20
N2 - 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.
AB - 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.
KW - Adipocyte size
KW - Ambient fine particles
KW - Gestational exposure
KW - Inflammatory response
KW - Lipid metabolism
UR - http://www.scopus.com/inward/record.url?scp=85058392986&partnerID=8YFLogxK
U2 - 10.1016/j.scitotenv.2018.12.007
DO - 10.1016/j.scitotenv.2018.12.007
M3 - Journal article
C2 - 30677905
AN - SCOPUS:85058392986
SN - 0048-9697
VL - 657
SP - 1389
EP - 1397
JO - Science of the Total Environment
JF - Science of the Total Environment
ER -
