Open AccessDevelopment of a fatty liver model using oleic acid in primary liver cells isolated from Atlantic salmon and the prevention of lipid accumulation using metformin
Author(s) -
Espe Marit,
Xie Shiwei,
Chen Shijun,
Pedro Araujo,
Holen Elisabeth
Publication year - 2019
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.12905
Subject(s) - metformin , cd36 , oleic acid , fatty liver , lipid droplet , biology , fatty acid , endocrinology , medicine , gene expression , lipid metabolism , biochemistry , gene , diabetes mellitus , disease
Abstract The following study aimed to develop a fatty liver model in primary hepatocytes isolated from Atlantic salmon. In order to induce the fatty liver, oleic acid (OA) at 0.2 or 0.4 mM was used. Metformin, known to prevent and cure fatty liver in mammalian cells, was used at 1 or 10 mM for 24 hr before addition of OA to test possible prevention effect of metformin on the OA‐induced fatty liver phenotype. Cells grown in 0.2 mM OA did not increase the mean number of lipid droplets, while cells grown in 0.4 mM OA increased the number of lipid droplets within the liver cells ( p < 0.0001). Metformin pretreatment prior to OA supplementation reduced the mean number of lipid droplets. Gene expression of ApoB100 , CD36 and PPARa increased in cells treated with metformin and most so at 10 mM. On the other hand, gene expression of LXR , SREBP2 and CPT‐1 decreased at both concentrations of metformin, while OA treatment did not affect these genes. Gene expression of IL‐8 increased by 0.4 mM OA ( p = 0.002). Metformin reduced the gene expression of IL‐8 . Thus, metformin efficiently enhanced the expression of genes related to transport and oxidation of lipids in hepatic cells of salmon, but required higher concentrations of OA and metformin than those required in rodent models to increase and prevent lipid accumulation, respectively.