Replacing fish meal with cottonseed meal protein hydrolysate affects amino acid metabolism via AMPK/SIRT1 and TOR signaling pathway of Megalobrama amblycephala

Abstract

This study was conducted to evaluate effects of replacing fish meal with cottonseed meal protein hydrolysate (CPH) on amino acid metabolism of Megalobrama amblycephala. Fish (38.66 ± 0.08 g) were randomly divided into five groups and fed five isonitrogenous (320 g kg−1 crude protein) and isocaloric (17.8 MJ kg−1 gross energy) diets replacing fish meal by CPH 0% (CPH 0), 1% (CPH 1), 3% (CPH 3), 5% (CPH 5) and 7% (CPH 7). Dietary 3% CPH had no effect on plasma aspartate aminotransferase (AST), alanine aminotransferase (ALT), succinate dehydrogenase (SDH) and xanthine oxidase (XOD) contents and liver SDH and XOD (P > 0.05), but significantly increased hepatic AST and ALT contents (P < 0.05). The plasma threonine (Thr), valine (Val), lysine (Lys), histidine (His), total essential amino acids and total amino acids contents of fish fed CPH5 and CPH7 diets significantly decreased (P < 0.05) compared with the control diet. Meanwhile, threonine (Thr), valine (Val), isoleucine (Ile) and leucine (Leu) contents in muscle significantly decreased (P < 0.05) when fish fed CPH7 diet. Diets with 5% and 7% CPH significantly decreased target of rapamycin (TOR) and S6 kinase-polypeptide 1 (S6K1) mRNA expressions levels in liver and gut, but increased eukaryotic translation initiation factor 4E-binding protein 2 (4E-BP2) mRNA expression levels (P < 0.05), as well as increased hepatic AMP-activated protein kinase α1 (AMPKa-1), AMP-activated protein kinase α2 (AMPKa-2) and sirtuin-1 (SIRT-1) mRNA expressions levels. Furthermore, the AMP-activated protein kinase α (t-AMPKα) and phospho-AMPKα (p-AMPKα) protein contents were increased significantly in fish fed with 5% and 7% CPH over the control group (P < 0.05). Overall, replacing fish meal with CPH at high level (5 and 7%) decreased the amino acid metabolism and growth performance, as well as inhibited ATP consumption via inhibiting TOR signaling pathway and activating AMPK/SIRT1 pathway.