This study was conducted to understand the effect of high‐fat diet challenge on lipid accumulation and inflammation in blunt snout bream. Fish (initial body weight: 41.84±0.07g) were fed a control diet or a high‐fat diet (HFD) for 9weeks, and the isolated primary hepatocytes were treated with 0.4mM oleic acid (OA) and/or 10ng/ml TNF‐α for 24hr. The results of the growth performance and feed utilization showed that short‐term feeding of HFD could increase energy intake and WGR, but long‐term feeding of HFD could inhibit feed intake. Hepatic steatosis and inflammation were observed in the HFD group according to enzyme activities or transcription levels of the related genes. In vitro, compared to untreated hepatocytes from fish fed a control diet, exposure of hepatocytes to OA could not only induce lipid accumulation but also promote pro‐inflammatory cytokines, such as TNF‐α and IL‐6. Increased fatty acid synthesis and decreased fatty acid oxidation were found in hepatocytes treated with TNF‐α alone, and co‐incubation of hepatocytes with OA and TNF‐α had a more substantial impact on lipid metabolism. Taken together, our results indicated that pro‐inflammatory cytokine TNF‐α was a crucial mediator of lipid accumulation in the liver of blunt snout bream fed HFD.

中文翻译：

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高脂饮食诱发的炎症通过脂肪酸合成和氧化的转录调控加重钝嘴鲷（Megalobrama amblycephala）的肝脂肪变性。

进行这项研究是为了了解高脂饮食挑战对钝嘴鲷的脂质积累和炎症的影响。给鱼类（初始体重：41.84±0.07g）喂食对照饮食或高脂饮食（HFD）9周，分离的原代肝细胞用0.4mM油酸（OA）和/或10ng / ml TNF处理-α24小时。生长性能和饲料利用率的结果表明，HFD的短期饲喂可以增加能量摄入和WGR，而HFD的长期饲喂可以抑制饲料摄入。根据酶活性或相关基因的转录水平，在HFD组中观察到肝脂肪变性和炎症。在体外，与饲喂对照饮食的鱼类未经处理的肝细胞相比，肝细胞暴露于OA不仅可以诱导脂质蓄积，而且可以促进促炎性细胞因子，例如TNF-α和IL-6。单独用TNF-α处理的肝细胞发现脂肪酸合成增加，而脂肪酸氧化减少，并且将肝细胞与OA和TNF-α共同孵育对脂质代谢的影响更大。综上所述，我们的结果表明促炎性细胞因子TNF-α是饲喂HFD的钝口鼻鲷肝脏中脂质积累的关键介质。