Prenatal exposure to diesel exhaust PM2.5 programmed non-alcoholic fatty liver disease differently in adult male offspring of mice fed normal chow and a high-fat diet. (December 2019)

• Record Type: Journal Article
• Authors: Wang, Xiaoke; Yang, Yuxue; Zhu, Piaoyu; Wu, Yifan; Jin, Yang; Yu, Shali; Wei, Haiyan; Qian, Muzhou; Cao, Weiming; Xu, Shenya; Liu, Yingqi; Chen, Gang; Zhao, Xinyuan
• Is Part Of: Environmental pollution. Volume 255(2019)Part 1
• Publication Date: 2019-12
• Subjects: Prenatal exposure -- DEP -- NAFLD -- Offspring; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2019.113366
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: Air pollution is one of the leading preventable threats to public health. Emerging evidence indicates that exposure to environmental stressors is associated with abnormal foetal development. However, how prenatal exposure to diesel exhaust PM2.5 (DEP) predisposes adult offspring to the development of non-alcoholic fatty liver disease (NAFLD) remains unclear. To examine this, C57BL/6J mice were exposed to DEP or a vehicle before conception and during pregnancy and fed normal chow or a high-fat diet. Then, the hepatic fatty accumulation in the adult male offspring and possible molecular mechanisms were assessed. Our data showed that prenatal exposure to DEP on normal chow led to hepatic steatosis in adult male offspring with normal liver function. However, prenatal DEP exposure relieved the hepatic steatosis and liver function in offspring of mice fed a high-fat diet. Furthermore, prenatal exposure to DEP on normal chow increased lipogenesis and worsened fatty acid oxidation. The counteractive effect of prenatal DEP exposure on high-fat-diet-induced hepatic steatosis was produced through upregulated adenosine 5′-monophosphate-activated protein kinase, and this improved lipogenesis and fatty acid oxidation. Collectively, prenatal exposure to DEP programmed the development of NAFLD differently in the adult male offspring of mice fed normal chow and a high-fat diet, showing the pleotrophic effects of exposure to adverse environmental factors in early life. Graphical abstract: Image 106380 Highlights: Prenatal exposure to DEP programmed the hepatic steatosis in adult male offspring. Prenatal exposure to DEP induced hepatic steatosis in offspring of mice fed normal chow food. Prenatal exposure to DEP alleviated the hepatic steatosis in offspring of mice fed high fat diet. SREBP-1c and PPAR-α pathway involved in the programming of steatosis induced by prenatal exposure to DEP. Abstract : Prenatal exposure to DEP induced hepatic steatosis in the offspring of mice on CF but alleviated steatosis and liver injuries in the offspring of mice fed a HF.