A 75‐day experiment was conducted with juvenile gibel carp (Carassius auratus gibelio) (4.80 ± 0.01 g) to evaluate effects of dietary chitosan on fish growth performance, haematology, intestine morphology and immune response. Six isonitrogenous (crude protein: 383 g kg⁻¹), isolipid (97.5 g kg⁻¹) and isocaloric (gross energy: 16.7 kJ g⁻¹) diets were formulated to contain 0, 1800, 4000, 7500, 10 000, 20 000 mg kg⁻¹ chitosan, respectively. The results showed that the growth was depressed when the fish fed with 10 000 mg kg⁻¹ chitosan. Serum cholesterol, triglyceride and low‐density lipoprotein decreased in 10 000 and 20 000 mg kg⁻¹ chitosan. On day 75, blood leucocyte phagocytic activity respiratory burst and alternative pathway of complement haemolytic activity were enhanced in 4000 mg kg⁻¹ chitosan. The number of goblet cell, intraepithelial lymphocyte of mid‐intestine and microvilli height of distal intestine increased at 4000 mg kg⁻¹ dietary chitosan. Dietary chitosan modulated intestine microbiota, depressed pathogen bacteria Aeromonas veronii‐like and improved Cellulomonas hominis‐like, Bacillus oceanisediminis‐like and two uncultured bacterium‐like species on day 75. Dietary 7500 and 10 000 mg kg⁻¹ chitosan enhanced the protection against Aeromonas hydrophila infection. In conclusion, oral administration of dietary 7500 mg kg⁻¹ chitosan for 75 days is recommended for the survival of gibel carp.

Triplicate groups of gibel carp Carassius auratus gibelio (initial body weight: 5.25 ± 0.02 g) were fed for 8 weeks at 20–25 °C on five isonitrogenous (crude protein: 400 g kg⁻¹) and isoenergetic diets (gross energy: 17 kJ g⁻¹). Meat and bone meal (MBM) or poultry by‐product meal (PBM) were used to replace fish meal at different levels of protein. The control diet contained fish meal as the sole protein source. In the other four diets, 150 or 500 g kg⁻¹ of fish meal protein was substituted by MBM (MBM₁₅, MBM₅₀) or PBM (PBM₁₅, PBM₅₀). The results showed that feeding rate for the MBM₅₀ group was significantly higher than for other groups except the PBM₅₀ group (P < 0.05). Growth rate in the MBM₁₅ group was significantly higher than that in the control (P < 0.05), while there was no significant difference in growth between the control and other groups (P > 0.05). Feed efficiency and protein efficiency ratio in MBM₅₀ was significantly lower while that in MBM₁₅ was significantly higher (P < 0.05). Replacement of fish meal by MBM at 500 g kg⁻¹ protein significantly decreased apparent dry matter digestibility (ADC_D) and gross energy (ADC_E) while apparent protein digestibility (ADC_P) was significantly decreased by the replacement of MBM or PBM (P < 0.05). The results suggest that MBM and PBM could replace up to 500 g kg⁻¹ of fish meal protein in diets for gibel carp without negative effects on growth while 150 g kg⁻¹ replacement by MBM protein improved feed utilization.

Previous studies have found that vitamin C (VC) has protective effects in fish. However, the efficacy of VC on hypoxia-induced liver injury in fish remains unknown. Therefore, to investigate the protective mechanism of VC on liver injury after acute hypoxic stimulation in fish, gibel carp were fed a diet containing VC for eight weeks, then were subjected to acute hypoxia stimulation. The specific growth rate of fish was increased by the supplementation of VC. Plasma stress markers (glucose, lactic acid, and cortisol) were decreased by the VC supplementation. Moreover, the levels of the inflammatory cytokines (tnf-α, il-2, il-6, and il-12) were increased by enhancing the Nrf2/Keap1 signaling pathway. Upregulation of the antioxidant enzymes activity (CAT, SOD, and GPx); T-AOC; and anti-inflammatory factors (il-4 and tgf-β) highlighted the antioxidant and anti-inflammatory activities of VC. The results showed that VC reduced the apoptotic index of the fish hypothalamus. The expression of GRP78 protein in the liver and endoplasmic reticulum stress and apoptosis induced by hypoxia were inhibited by VC. Taken together, the results indicate that VC can attenuate oxidative damage, inflammation, and acute hypoxia induced apoptosis in gibel carp via the Nrf2/Keap1 signaling pathway. The results identify a new defense strategy of gibel carp in response to hypoxic conditions.