Journal
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume 90, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.etap.2022.103808
Keywords
Decabromodiphenyl ether; Glycolipid metabolism; PKA; AMPK signaling pathway; PRKACA; DNA hypermethylation
Funding
- National Natural Science Foundation of China [31770441]
- Graduation Project of Practical Training Plan (Scientific Research) about Cross-training of high-level talents in Beijing institutions of higher learning
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This study found that BDE-209 induces liver tissue injury and disrupts glycolipid metabolism. It alters the expression of proteins related to the PKA/AMPK signaling pathway in the liver and cells. BDE-209 also causes hypermethylation of PRKACA-1, which is involved in regulating this pathway.
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 L02 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.
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