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A 100‐day feeding trial was conducted to investigate the influences of dietary lipid levels on the immunity and mechanism in abalone Haliotis discus hannai Ino. Abalones (initial weight: 10.98 ± 0.05 g) were fed with graded levels of dietary lipid, which were 15.73, 23.41, 31.72, 38.25, 46.35, 55.63, 61.70 and 67.19 g/kg. Results showed that compared with the treatment with 38.25 g/kg of dietary lipid, 67.19 g/kg of dietary lipid increased the cumulative mortality of abalone after a challenge with Vibrio parahaemolyticus. Meanwhile, 67.19 g/kg of dietary lipid decreased the activities of lysozyme (LZ) and acid phosphatase (ACP) in serum, and the mRNA levels of β‐defensin and mytimacin 6 in hepatopancreas of abalone. The mRNA levels of tumour necrosis factor α (tnfα), activator protein 1 (ap‐1), nuclear factor κB (nf‐κb), interleukin 1 receptor‐associated kinase‐4 (irak4), myeloid differentiation primary response protein MyD88 (myd88), toll‐like receptor 2 (tlr2), tlr4 and perilipin‐2, and the protein level of interleukin‐1β (IL‐1β), TNFα, NF‐κBp65, AP‐1, MyD88 and Perilipin‐2 in hepatopancreas were up‐regulated by 67.19 g/kg of dietary lipid. However, the mRNA levels of arginase and inhibitor of κBα (iκbα) were down‐regulated. Besides, 67.19 g/kg of dietary lipid up‐regulated the mRNA levels of executor apoptosis‐related cysteine peptidase 3 (caspase‐3), caspase‐7 and B‐cell lymphoma protein‐2‐associated X protein (bax), and the protein levels of caspase‐3 and c‐Jun N‐terminal kinases (JNK) in hepatopancreas. Moreover, high dietary lipid level down‐regulated the mRNA levels of copper/zinc superoxide dismutase (cuznsod), manganese superoxide dismutase (mnsod), catalase (cat), glutathione peroxidase (gpx), glutathione‐S‐transferase (gst) and NF‐E2‐related factor 2 (nrf2), while up‐regulated the mRNA and protein levels of Kelch‐like ECH‐associated protein 1 (Keap1) in hepatopancreas. It was concluded that a high level (67.19 g/kg) of dietary lipid decreased the immunity of abalone, which might be related to the aggravated inflammation and apoptosis, and decreased anti‐oxidative capacity under Perilipin‐2/TLRs/MyD88/IRAK4/(NF‐κB or AP‐1), JNK/Bcl‐2/Bax and Keap1/Nrf2 signalling. [ABSTRACT FROM AUTHOR]

Arginine plays an important role in the regulation of the target of the rapamycin (TOR) signaling pathway, and Solute Carrier Family 38 Member 9 (SLC38A9) was identified to participate in the amino acid-dependent activation of TOR in humans. However, the regulations of arginine on the TOR signaling pathway in abalone are still unclear. In this study, slc38a9 of abalone was cloned, and the slc38a9 was knocked down and overexpressed to explore its function in the regulation of the TOR signaling pathway. The results showed that knockdown of slc38a9 decreased the expression of tor, ribosomal s6 protein kinase (s6k) and eukaryotic translation initiation factor 4e (eif4e) and inhibited the activation of the TOR signaling pathway by arginine. Overexpression of slc38a9 up-regulated the expression of TOR-related genes. In addition, hemocytes of abalone were treated with 0, 0.2, 0.5, 1, 2 and 4 mmol/L of arginine, and abalones were fed diets with 1.17%, 1.68% and 3.43% of arginine, respectively, for 120 days. Supplementation of arginine (0.5–4 mmol/L) increased the expressions of slc38a9, tor, s6k and eif4e in hemocytes, and abalone fed with 1.68% of dietary arginine showed higher mRNA levels of slc38a9, tor, s6k and eif4e and phosphorylation levels of TOR, S6 and 4E-BP. In conclusion, the TOR signaling pathway of abalone can be regulated by arginine, and SLC38A9 plays an essential role in this regulation. [ABSTRACT FROM AUTHOR]

Clostridium autoethanogenum protein (CAP) is an eco-friendly protein source and has great application potential in aquafeeds. The present study aimed to investigate the effects of dietary CAP inclusion on the anti-oxidation, immunity, inflammation, disease resistance and gut microbiota of abalone Haliotis discus hannai after a 110-day feeding trial. Three isonitrogenous and isolipidic diets were formulated by adding 0 % (control), 4.10 % (CAP4.10) and 16.25 % (CAP16.25) of CAP, respectively. A total of 540 abalones with an initial mean body weight of 22.05 ± 0.19 g were randomly distributed in three groups with three replicates per group and 60 abalones per replicate. Results showed that the activities of superoxide dismutase and glutathione peroxidase in the cell-free hemolymph (CFH) were significantly decreased and the content of malondialdehyde in CFH was significantly increased in the CAP16.25 group. The diet with 4.1 % of CAP significantly increased the activities of lysozyme and acid phosphatase in CFH. The expressions of pro-inflammatory genes such as tumor necrosis factor-α (tnf-α), nuclear factor-κb (nf-κb) and toll-like receptor 4 (tlr4) in digestive gland were downregulated, and the expressions of anti-inflammatory genes such as β-defensin and mytimacin 6 in digestive gland were upregulated in the CAP4.10 group. Dietary CAP inclusion significantly decreased the cumulative mortality of abalone after the challenge test with Vibrio parahaemolyticus for 7 days. Dietary CAP inclusion changed the composition of gut microbiota of abalone. Besides, the balance of the ecological interaction network of bacterial genera in the intestine of abalone was enhanced by dietary CAP. The association analysis showed that two bacterial genera Ruegeria and Bacteroides were closely correlated with the inflammatory genes. In conclusion, the 4.10 % of dietary CAP enhanced the immunity and disease resistance as well as inhibited the inflammation of abalone. The 16.25 % of dietary CAP decreased the anti-oxidative capacity of abalone. The structure of the gut microbiota of abalone changed with dietary CAP levels. [Display omitted] • Low dietary Clostridium autoethanogenum (CAP) inclusion (4.1 %) improved the immunity of abalone. • It also improved the resistance of abalone against V. parahaemolyticus infection. • The 4.1 % of dietary CAP decreased the inflammation of abalone. • High dietary CAP level (16.25 %) decreased the anti-oxidative capacity of abalone. • The composition and structure of the gut microbiota of abalone changed with dietary CAP levels. [ABSTRACT FROM AUTHOR]

A 110-day feeding trial was carried out to investigate the impacts of replacing dietary fish meal (FM) with poultry by-product meal (PBM) on growth performance, digestion, gut microbiota, immunity, and disease resistance of abalone Haliotis discus hannai (initial weight: 22.53 ± 0.21 g). The control diet (PBM0) without PBM contained 20% of FM. Based on PBM0, the other four isonitrogenous (about 30% of crude protein) and isolipidic (about 4% of crude lipid) diets were formulated replacing 25, 50, 75 and 100% of FM by PBM (designated as PBM25, PBM50, PBM75 and PBM100), respectively. Every diet was fed to triplicate cages (40 × 35 × 70 cm) with 60 abalones per cage. At the end of the feeding trial, abalones were starved for 3 days and anesthetized with 5% ethanol before sampling. Results indicated that biomass gain of the abalone fed PBM75 (916.71 g) and PBM100 (659.93 g) was significantly lower than that of the abalone fed PBM0 (1222.51 g). Feed conversion ratio of the abalone fed PBM50 (2.93), PBM75 (2.89) and PBM100 (4.04) were significantly higher than that of the abalone fed PBM0 (2.37). The muscle crude protein content of the abalone fed PBM100 (16.01% wet weight) was significantly lower than that of the abalone fed PBM0 (16.67% wet weight). Activities of trypsin and α-amylase in the digestive gland in the PBM100 group (309.21 and 0.064 U/mg prot., respectively) were significantly lower than the PBM0 group (463.57 and 0.078 U/mg prot., respectively). When the substitution levels rose over 50%, expressions of phosphatidylinositol 3 kinase, threonine kinase/protein B, mammalian target of rapamycin and eukaryotic translation initiation factor 4E in muscle were significantly reduced, while 4E binding protein was significantly increased. The most abundant phyla across the abalones' gut were Proteobacteria and Firmicutes. Catalase (from 2.90 to 1.69 U/mL), superoxide dismutase (from 98.93 to 74.39 U/mL), lysozyme (from 345.86 to 247.81 U/mL) and acid phosphatase (from 21.68 to 15.71 U/100 mL) activities in cell-free hemolymph were markedly decreased with substitution level increasing. When the replacement levels rose over 50%, myeloid differentiation primary response gene 88 and tumor necrosis factor α expressions in the digestive gland were markedly upregulated, while β-defensin and mytimacin 6 expressions were markedly downregulated. The cumulative mortality of abalone challenged with Vibrio parahaemolyticus (1.0 × 107 CFU/mL) for 7 days was remarkably increased in the PBM50 (83.49%), PBM75 (89.56%) and PBM100 (100%) groups compared with the PBM0 group (58.82%). In conclusion, 50% of dietary FM could be replaced by PBM without influencing abalone growth. When the replacement level was over 50%, the growth and immunity of abalone were decreased, and the mTOR pathway was negatively affected. • Replacement of dietary fishmeal (FM, 0–20%) by poultry by-product meal (PBM, 0–20.5%) was evaluated in abalone. • The control diet was formulated with 20% of FM and without PBM. • There were no adverse effects on growth when replacement was 50% or less. • Negative effects on growth, immunity and disease resistance were found when PBM replaced more than 50% of FM. • The PBM can be used as an important protein source in the diet for abalone. [ABSTRACT FROM AUTHOR]

The present study investigated the effects of different dietary carbohydrate levels on the growth performance, body composition, glucose/lipid metabolism and insulin signaling pathway in abalone Haliotis discus hannai. Eight experimental diets with graded levels of carbohydrates (18.08%, 22.10%, 26.10%, 29.90%, 34.00%, 38.01%, 41.98% and 45.55%, named as T1, T2, T3, T4, T5, T6, T7 and T8, respectively) were designed to feed abalone (initial weight 22.52 ± 0.05 g) for 110 days. The results showed that the diet containing 38.01% carbohydrate significantly increased the survival rate (SR) and weight gain rate (WGR) of abalone (P < 0.05). Based on the quadratic regression mode of WGR, the optimal dietary carbohydrate level for abalone was estimated to be 37.05%. The activities of intestinal digestive enzymes were significantly increased in the T6 group. Moreover, the expressions of pyruvate kinase (pk) and glucose-6-phosphate dehydrogenase (g6pdh) in digestive glands were up-regulated with the increase of carbohydrate content in diets, while the expression of hexokinase (hk) reached the maximum in the T6 group. The highest expressions of phosphoenolpyruvate carboxykinase (pepck), glucose-6-phosphatase (g6pase) and insulin signaling pathway related genes were found in the T6 group. The expressions of key genes related to lipolysis reached the highest in the T6 group, and then down-regulated with the further increasing dietary carbohydrate levels. The expression of key genes of lipogenesis was up-regulated with the increasing dietary carbohydrate levels. In conclusion, 38.01% of dietary carbohydrate level improved the growth performance of abalone. Dietary carbohydrate levels influenced the glucose and lipid metabolism including insulin signaling pathway. Abalone potentially had the capability to deal with a high-carbohydrate load (45.55%) by increasing glycolysis and decreasing gluconeogenesis. Meanwhile, it promoted lipid synthesis and inhibited lipolysis under high dietary carbohydrate load. • The dietary carbohydrate requirement of abalone was estimated to be 37.05%. • Deficient (18.10%) or excessive (45.55%) dietary carbohydrate content decreased the growth of abalone. • Appropriate dietary carbohydrate content increased the digestive enzyme activities in abalone. • Dietary carbohydrate levels increased the crude lipid content in the soft body of abalone. • Glucose and lipid metabolism including the insulin signaling pathway were regulated by dietary carbohydrate levels. [ABSTRACT FROM AUTHOR]