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Decabromodiphenyl ether-induced PRKACA hypermethylation contributed to glycolipid metabolism disorder via regulating PKA/AMPK pathway in rat and L-02 cells
Zhu, Yupeng1,2,3; Jing, Li1,2; Li, Xiangyang1,2; Zhou, Guiqing1,2; Zhang, Yue1,2; Sang, Yujian1,2; Gao, Leqiang1,2; Liu, Sitong1; Shi, Zhixiong1,2; Sun, Zhiwei1,2; Ge, Wei4; Zhou, Xianqing1,2
2022-02-01
Source PublicationEnvironmental Toxicology and Pharmacology
ISSN1382-6689
Volume90
Abstract

BDE-209 is the most prevalent congener of polybrominated diphenyl ethers and has high bioaccumulation in humans and animals. BDE-209 has been reported to disrupt glycolipid metabolism, but the mechanisms are still unclear. In this study, we found that BDE-209 induced liver tissue injury and hepatotoxicity, increased the glucose and total cholesterol levels in the serum of rats, and increased glucose and triglyceride levels in L-02 cells. BDE-209 exposure changed the PKA, p-PKA, AMPK, p-AMPK, ACC, and FAS expression in rats’ liver and L-02 cells. Moreover, BDE-209 induced PRKACA-1 hypermethylation in L-02 cells. AMPK activator (AICAR) inhibited the changes of p-AMPK, ACC, and FAS expression and elevation of glucose and triglyceride levels induced by BDE-209. DNA methylation inhibitor (5-Aza-CdR) reversed BDE-209 induced alters of PKA/AMPK/ACC/FAS signaling pathway. These results demonstrated that BDE-209 could disrupt the glycolipid metabolism by causing PRKACA-1 hypermethylation to regulate the PKA/AMPK signaling pathway in hepatocytes.

KeywordDecabromodiphenyl Ether Dna Hypermethylation Glycolipid Metabolism Pka/ampk Signaling Pathway Prkaca
DOI10.1016/j.etap.2022.103808
URLView the original
Indexed BySCIE
Language英語English
WOS Research AreaEnvironmental Sciences & Ecology ; Pharmacology & Pharmacy ; Toxicology
WOS SubjectEnvironmental Sciences ; Pharmacology & Pharmacy ; Toxicology
WOS IDWOS:000788052300003
Scopus ID2-s2.0-85123238025
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Document TypeJournal article
CollectionFaculty of Health Sciences
Corresponding AuthorGe, Wei; Zhou, Xianqing
Affiliation1.Department of Toxicology and Hygienic Chemistry, School of Public Health, Capital Medical University, Beijing, 100069, China
2.Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, China
3.Haidian Maternal&Child Health Hospital, Health Care Department for Women, Beijing, 100080, China
4.Centre of Reproduction, Development and Aging (CRDA), Faculty of Health Sciences, University of Macau, Taipa, 999078, China
Corresponding Author AffilicationCentre of Reproduction, Development and Aging
Recommended Citation
GB/T 7714
Zhu, Yupeng,Jing, Li,Li, Xiangyang,et al. Decabromodiphenyl ether-induced PRKACA hypermethylation contributed to glycolipid metabolism disorder via regulating PKA/AMPK pathway in rat and L-02 cells[J]. Environmental Toxicology and Pharmacology,2022,90.
APA Zhu, Yupeng,Jing, Li,Li, Xiangyang,Zhou, Guiqing,Zhang, Yue,Sang, Yujian,Gao, Leqiang,Liu, Sitong,Shi, Zhixiong,Sun, Zhiwei,Ge, Wei,&Zhou, Xianqing.(2022).Decabromodiphenyl ether-induced PRKACA hypermethylation contributed to glycolipid metabolism disorder via regulating PKA/AMPK pathway in rat and L-02 cells.Environmental Toxicology and Pharmacology,90.
MLA Zhu, Yupeng,et al."Decabromodiphenyl ether-induced PRKACA hypermethylation contributed to glycolipid metabolism disorder via regulating PKA/AMPK pathway in rat and L-02 cells".Environmental Toxicology and Pharmacology 90(2022).
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