Integrated metabolomics and proteomics analysis to provide insights into muscle atrophy of turbot Scophthalmus maximus by dietary Clostridium autoethanogenum protein

Abstract

Clostridium autoethanogenum protein (CAP) is a promising protein source for aquaculture. Previous studies proved that high levels of dietary CAP retarded the muscle development in turbot through mammalian target of rapamycin (mTOR)/amino acid response (AAR)/adenosine monophosphate-activated protein kinase (AMPK) pathways. However, how CAP regulating these pathways was still unclear and there was no information on the comprehensive analysis for the mechanisms of CAP on fish muscle. In the present study, the integration of metabolomic and proteomic was applied on the muscle of turbot (initial weight of 150 ± 3 g) fed with fishmeal-based diet or diet with 60 % of fishmeal protein replaced by CAP for 70 days. The present work confirmed that CAP decreased the growth, fillet yield and induced the muscle atrophy. Integrated analysis of metabolomics and proteomics showed that CAP negatively influenced the energy production by inhibiting the key enzymes of glycolysis and mitochondrial respiratory chain. Second, CAP inhibited mitogen-activated protein kinase (MAPK) and phosphatidylinositol-3-kinase (PI3K) pathways to down-regulate mTOR pathways and protein synthesis. Third, the amino acid contents in turbot muscle were imbalanced by CAP, which would be perceived by general control nonderepressible 1 in AAR signal pathways. Finally, the up-regulated AAR induced amino acids catabolism through purine-based combined deamination. In conclusion, the present work provided the universal knowledge on the working principle of CAP and laid the foundation for CAP improvement in the future.

Keywords

• Clostridium autoethanogenum protein
• Turbot
• Glycolysis
• Oxidative phosphorylation
• Protein deposition