Effects of sodium acetate on lipid metabolism, antioxidant capability and cell apoptosis of blunt snout bream ( <i>Megalobrama amblycephala</i> ) hepatocytes treated by sodium palmitate

Abstract

The present study aimed to figure out whether high-fat diet could change the contents of SCFAs in the intestine and the effects of such changes on fatty liver diseases in Megalobrama amblycephala. The results showed that acetate concentration in the intestinal tissue and chyme of M. amblycephala was decreased when fish fed high-fat diet (10% dietary fat) than that fed normal diet (5% dietary fat). Then, effects of sodium acetate (SA) on lipid metabolism, antioxidant capability and apoptosis of M. amblycephala hepatocytes treated by sodium palmitate (SP) were elucidated. It was showed that SP significantly increased cell damages, lipid accumulation, oxidative stress and apoptosis (p < 0.05). SA could reduce cell damages by decreasing the aspartate aminotransferase (AST) activity (p < 0.05), attenuate oxidative stress through reducing intracellular oxygen species (ROS) and malondialdehyde (MDA) contents (p < 0.05), alleviate lipid accumulation by decreasing total cholesterol (TC) and non-esterified fatty acids (NEFA) contents (p < 0.05), along with down-regulating acetyl CoA carboxylase (ACC) activity and up-regulating carnitine palmitoyltransferase 1 (CPT-1) mRNA expression (p < 0.05). In addition, SA increased mitochondrial membrane potential and reduced cell apoptosis caused by SP treatment. Transmission electron microscopy found that the structures of karyotheca, endoplasmic reticulum and mitochondria in hepatocytes were badly damaged by SP and then repaired by SA. Our findings may provide new ideas and basis for high-fat diet and SCFAs (acetate) used in aquaculture practice.