Open AccessHigh‐fat diet‐induced inflammation aggravates hepatic steatosis of blunt snout bream ( Megalobrama amblycephala ) through the transcription regulation of fatty acid synthesis and oxidation
Author(s) -
Cao XiuFei,
Liu WenBin,
Ai QingHui,
Li XueShan,
Li JinBao,
Fang Wei,
Huang YangYang,
Wang CongCong,
Jiang GuangZhen
Publication year - 2020
Publication title -
aquaculture nutrition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.941
H-Index - 79
eISSN - 1365-2095
pISSN - 1353-5773
DOI - 10.1111/anu.13097
Subject(s) - megalobrama , steatosis , biology , lipid metabolism , medicine , endocrinology , inflammation , fatty acid , fatty liver , oleic acid , biochemistry , immunology , disease , gene
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.