Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China; International Joint Research Laboratory for Fish Immunopharmacology, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China.
Key Laboratory of Freshwater Fisheries and Germplasm Resources Utilization, Ministry of Agriculture and Rural Affairs, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China; International Joint Research Laboratory for Fish Immunopharmacology, Freshwater Fisheries Research Center, Chinese Academy of Fishery Sciences, Wuxi, 214081, China.
Fish Shellfish Immunol. 2020 Sep;104:391-401. doi: 10.1016/j.fsi.2020.06.025. Epub 2020 Jun 14.
Fatty liver injury (or disease) is a common disease in farmed fish, but its pathogenic mechanism is not fully understood. Therefore the present study aims to investigate high-fat diet (HFD)-induced liver injury and explore the underlying mechanism in fish. The tilapia were fed on control diet and HFD for 90 days, and then the blood and liver tissues were collected to determine biochemical parameter, gene expression and protein level. The results showed that HFD feeding signally increased the levels of plasma aminotransferases and pro-inflammatory factors after 60 days. In liver and plasma, HFD feeding significantly suppressed antioxidant ability, but enhanced lipid peroxidation formation, protein oxidation and DNA damage after 60 or 90 days. Further, the Nrf2 pathway and antioxidative function-related genes were adversely changed in liver of HFD-fed tilapia after 60 and/or 90 days. Meanwhile, HFD treatment induced apoptosis via initiating mitochondrial pathway in liver after 90 days. Furthermore, after 90 days of feeding, the expression of genes or proteins related to JNK pathway and TLRs-Myd88-NF-κB pathway was clearly upregulated in HFD treatment. Similarly, the mRNA levels of inflammatory factors including tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), IL-6, IL-8 and IL-10 were also upregulated in liver of HFD-fed tilapia after 60 and/or 90 days. In conclusion, the current study suggested that HFD feeding impaired antioxidant defense system, induced apoptosis, enhanced inflammation and led to liver injury. The adverse influences of HFD in the liver might be due to the variation of Nrf2, JNK and TLRs-Myd88-NF-κB signaling pathways.
脂肪肝损伤（或疾病）是养殖鱼类的一种常见疾病，但其发病机制尚未完全阐明。因此，本研究旨在探讨高脂肪饮食（HFD）诱导的鱼类肝损伤及其潜在机制。将罗非鱼分别用基础饲料和 HFD 喂养 90 天，然后采集血液和肝脏组织，测定生化参数、基因表达和蛋白水平。结果表明，HFD 喂养 60 天后可显著提高血浆转氨酶和促炎因子水平。在肝脏和血浆中，HFD 喂养 60 或 90 天后，显著抑制抗氧化能力，但增强脂质过氧化形成、蛋白质氧化和 DNA 损伤。进一步研究发现，HFD 喂养 60 和/或 90 天后，HFD 组罗非鱼肝组织中 Nrf2 通路和抗氧化功能相关基因发生了不利变化。同时，HFD 处理 90 天后诱导了肝脏中线粒体凋亡途径的激活。此外，90 天喂养后，HFD 处理组 JNK 通路和 TLRs-Myd88-NF-κB 通路相关基因或蛋白的表达明显上调。同样，HFD 喂养 60 和/或 90 天后，肝脏中炎性因子（TNF-α、IL-1β、IL-6、IL-8 和 IL-10）的 mRNA 水平也明显上调。综上所述，本研究表明 HFD 喂养破坏了抗氧化防御系统，诱导了细胞凋亡，增强了炎症反应，导致了肝损伤。HFD 对肝脏的不利影响可能与 Nrf2、JNK 和 TLRs-Myd88-NF-κB 信号通路的变化有关。
