This study aimed to determine the effects of dietary sodium butyrate (NaB) on the growth and gut health of triploid Oncorhynchus mykiss juveniles (8.86 ± 0.36 g) fed a low fish meal diet for 8 weeks, including the inflammatory response, histomorphology, and the composition and functional prediction of microbiota. Five isonitrogenous and isoenergetic practical diets (15.00% fish meal and 21.60% soybean meal) were supplemented with 0.00% (G1), 0.10% (G2), 0.20% (G3), 0.30% (G4), and 0.40% NaB (G5), respectively. After the feeding trial, the mortality for G3 challenged with Aeromonas salmonicida for 7 days was lower than that for G1 and G5. The optimal NaB requirement for triploid O. mykiss based on weight gain rate (WGR) and the specific growth rate (SGR) was estimated to be 0.22% and 0.20%, respectively. The activities of intestinal digestive enzymes increased in fish fed a NaB diet compared to G1 (p < 0.05). G1 also showed obvious signs of inflammation, but this inflammation was significantly alleviated with dietary NaB supplementation. In comparison, G3 exhibited a more complete intestinal mucosal morphology. Dietary 0.20% NaB may play an anti-inflammatory role by inhibiting the NF-κB-P65 inflammatory signaling pathway. Additionally, the relative abundance of probiotics was altered by dietary NaB. In conclusion, dietary 0.20% NaB improved the intestinal health of triploid O. mykiss fed a low fish meal diet.

Ammonia is a common environmental limiting factor in aquaculture. To investigate the effects of ammonia stress and explore the protective effect of N-carbamylglutamate (NCG) on Micropterus salmoides (M. salmoides), tissue sections and parameters related to oxidative stress and the inflammatory response in M. salmoides were carried out during the ammonia stress test and feeding test. The results demonstrated that the LC50 for 24 h, 48 h, 72 h, and 96 h under ammonia stress in M. salmoides were 25.78 mg/L, 24.40 mg/L, 21.90 mg/L, and 19.61 mg/L, respectively. Under ammonia stress, the structures of the tissues were damaged, and the GSH content decreased, while the MDA content increased with the increase in stress time and ammonia concentration. The NO content fluctuated significantly after the ammonia nitrogen stress. In the 15-day feeding test, with the increased NCG addition amount and feeding time, the GSH content increased while the MDA and NO contents decreased gradually in the NCG addition groups (NL group: 150 mg/kg; NM group: 450 mg/kg; NH group: 750 mg/kg) when compared with their control group (CK group: 0 mg/kg). In the ammonia toxicology test after feeding, the damage to each tissue was alleviated in the NL, NM, and NH groups, and the contents of GSH, MDA, and NO in most tissues of the NH group were significantly different from those in the CK group. The results suggested that ammonia stress caused tissue damage in M. salmoides, provoking oxidative stress and inflammatory response. The addition of NCG to the feed enhances the anti-ammonia ability of M. salmoides. Moreover, the gill and liver might be the target organs of ammonia toxicity, and the brain and kidney might be the primary sites where NCG exerts its effects. Our findings could help us to find feasible ways to solve the existing problem of environmental stress in M. salmoides culture.