Transcriptome analysis reveals the feeding response and oxidative stress in juvenile Micropterus salmoides fed a low-fish-meal diet with enzyme-hydrolysed intestinal mucosa protein substitution

Abstract

A 95-day feeding experiment was designed to evaluate the effects of fish meal with enzyme-hydrolysed intestinal mucosa protein (EMP) replacement of 0% (EMP0), 6.7% (EMP6.7), 13.3% (EMP13.3), 20.0% (EMP20.0), and 26.7% (EMP26.7) in Micropterus salmoides (M. salmoides). No negative effects were observed in the diet in which fish meal was replaced by EMP with 6.7%–13.3%, according to the growth and feed utilization indicators. Interestingly, food intake (FI) increased significantly with the replacement level of EMP. Transcriptome analysis showed that compared with the brains of M. salmoides fed the EMP0 diet, the brains of M. salmoides fed a low-fish-meal diet (EMP26.7) exhibited 1405 differentially expressed genes (DEGs), including 829 upregulated DEGs and 576 downregulated DEGs. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment indicated that EMP26.7 promoted the feeding of M. salmoides primarily by upregulating orexigenic factors and downregulating anorexigenic factors. The ingestion-related factors pomc, cck, and lpar1 were significantly correlated. Furthermore, GO and KEGG enrichment showed that long-term consumption of a low- fish-meal diet (EMP26.7) significantly affected oxidative stress and inflammation-related factors in the brain. Antioxidant indicators, including SOD, GSH, and T-AOC, were significantly downregulated, and MDA content was significantly upregulated in the brains of fish fed a low-fish-meal diet (EMP26.7 diet). SOD, GSH, and T-AOC were significantly correlated with epi-1 and negatively correlated with tlr13 and nod1. Negative relationships were found between MDA and epi-1, and positive relationships were found between nod1 and aqp3. In conclusion, the EMP could replace 6.7%–13.3% fish meal in the diet of M. salmoides without adversely affecting growth performance. The feeding response of M. salmoides to a low-fish-meal diet is to increase FI through the related feeding regulators in neuroactive ligand-receptor interaction, and a low-fish-meal diet can cause oxidative stress in the brain.