Hydrolysate of a low-carbon microbe protein improved the performance and antioxidant capacity in Micropterus salmoides

Low-fishmeal diets (LFM) represent a promising strategy for sustainable aquaculture, yet their practical efficacy remains inconsistent. Clostridium autoethanogenum protein hydrolysate (CAPH), derived from a low-carbon microbial protein with potential physiological regulatory functions, was evaluated in this study. We investigated graded CAPH supplementation (1.5 % and 3 %) in an LFM diet (24 % fishmeal) for largemouth bass, using a high-fishmeal control diet (HFM, 30 % fishmeal) as the benchmark. Results indicated that the LFM group achieved growth performance and physiological indices comparable to the HFM, confirming baseline adaptability to reduced fishmeal content. Notably, dietary 1.5 % CAPH significantly improved growth, while decreasing the feed conversion ratio. Further analysis revealed that CAPH improved intestinal morphological characteristics and enhanced the activity of intestinal digestive enzymes (alkaline phosphatase, trypsin, and amylase). CAPH addition upregulated the mRNA level of genes related to intestinal peptide transport (pept1 and pept2) and amino acid transport (lat1, lat2, sant2, and sant4), corresponding with increased plasma amino acid concentrations. Additionally, CAPH (1.5 %) activated hepatic mTOR signaling, evidenced by elevated mRNA level of mtor, alongside reduced 4e-bp1 gene expression. CAPH enhances antioxidant responses by reducing reactive oxygen species (ROS) and increasing total antioxidant capacity (T-AOC) and superoxide dismutase (SOD) activity. Accordingly, the activated hepatic Nrf2-keap1 signaling were observed in CAPH groups. These findings demonstrate that dietary fishmeal reduction from 30 % to 24 % maintained comparable growth performance in largemouth bass. In comparison, CAPH supplementation optimally enhances growth performance, feed utilization, and antioxidant capacity through coordinated regulation of digestive function, peptide/amino acid transport, Nrf2-keap1, and mTOR pathways.