Polybrominated diphenyl ethers (PBDEs) are widely present in water ecosystems where they pose a significant threat to aquatic life, but our knowledge about how PBDEs affect feeding is limited. Therefore, this study explored the effects of continuous dietary exposure to 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) (40 and 4000 ng/g) on the feeding in common carp () and the underlying mechanism. BDE-47 significantly decreased the food intake of carp. Transcriptome analysis of brain tissue showed that BDE-47 mainly affected the nervous, immune, and endocrine systems. Further examination of the expression levels of appetite factors in the brain revealed that BDE-47 caused dysregulation of appetite factors expressions such as , , , etc. In addition, the JAK-STAT signaling pathway was activated under BDE-47 exposure. It can be concluded from these findings that BDE-47 activated the JAK-STAT signaling pathway, causing imbalanced expression of appetite factors, leading to disordered feeding behavior and decreased food intake in carp. These results provide an important reference for a more comprehensive understanding of the hazards posed by BDE-47 on animal feeding and the associated mechanisms.

中文翻译：

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长期膳食暴露于 2,2',4,4'-四溴二苯醚 (BDE-47) 会减少鲤鱼 (Cyprinus carpio) 的摄食：通过 JAK-STAT 信号通路

多溴二苯醚 (PBDE) 广泛存在于水生态系统中，对水生生物构成重大威胁，但我们对 PBDE 如何影响摄食的了解有限。因此，本研究探讨了膳食中持续暴露于2,2',4,4'-四溴二苯醚（BDE-47）（40和4000 ng/g）对鲤鱼摄食的影响及其潜在机制。 BDE-47 显着降低鲤鱼的摄食量。脑组织转录组分析表明，BDE-47 主要影响神经、免疫和内分泌系统。进一步检查大脑中食欲因子的表达水平发现，BDE-47导致食欲因子表达失调，例如，，，等。此外，JAK-STAT信号通路在BDE-47暴露下被激活。从这些发现可以得出结论，BDE-47激活了JAK-STAT信号通路，导致食欲因子表达失衡，导致鲤鱼摄食行为紊乱和食物摄入量减少。这些结果为更全面地了解BDE-47对动物饲养造成的危害及其相关机制提供了重要参考。