Hepatic lipid metabolism and oxidative stress responses of grass carp (Ctenopharyngodon idella) fed diets of two different lipid levels against Aeromonas hydrophila infection

Abstract

The present study was conducted to investigate the effect of Aeromonas hydrophila infection and different lipid level diets on the performance, hepatic lipid metabolism, and oxidative stress in grass carp (Ctenopharyngodon idella). To this end, grass carp (50.73 ± 3.17 g) were divided into 4 groups: control group, A. hydrophila group, high-fat diet group, high-fat diet + A. hydrophila group for 8 weeks. Compared with the control group, there was no significant difference in hepatic lipid content in the A. hydrophila group for 8 weeks, but it increased significantly in 4 weeks. The results showed that A. hydrophila infection and feeding with basal diet may have influenced hepatic lipid deposition in a time-dependent manner. The expression of lipid decomposition-related gene adipose triacylglyceride lipase (ATGL) and lipoprotein lipase (LPL) were reduced at 4 weeks, and lipid synthesis-related gene fatty acid synthase (FAS), acetyl-CoA carboxylase α (ACCα), and stearoyl-CoA desaturase (SCD) were suppressed at 8 weeks, which reduced the lipid metabolism of the liver. Compared with the high-fat diet group, the hepatic lipid content was significantly increased in high-fat diet + A. hydrophila group for 8 weeks, indicating that A. hydrophila infection aggravated hepatic lipid deposition induced by high-fat diet, the expression of ACCα and FAS were significantly up-regulated, and lipid decomposition-related genes (ATGL, LPL, CPT1) were not significantly changed, indicating that A. hydrophila infection of grass carp fed with a high-fat diet could increase liver lipid synthesis. Oil red O staining and the relative area of lipid droplets further support this finding. Moreover, in both groups, A. hydrophila infection enhanced serum aspartate transaminase (AST), which was found to cause liver injury. Total antioxidant capacity (T-AOC) was reduced and malondialdehyde (MDA) content was increased in the liver after infection of A. hydrophila in both basal diet and high-fat diet groups, indicating that A. hydrophila infection weakened the antioxidant defense ability of the liver, which led to the occurrence of oxidative stress and oxidative damage to the liver. Our results indicated that dysregulation of hepatic lipid metabolism and damage of the antioxidant system in grass carp could be caused by challenge to a certain dose of A. hydrophila, and hepatic lipid deposition induced by A. hydrophila infection was closely related to dietary lipid content.