A 12‐week feeding trial was conducted to investigate the protective effects of arginine on the intestinal health of juvenile turbot (Scophthalmus maximus L.) fed high doses of dietary soybean meal. Sextuple replicates of 30 fish were fed each of four isonitrogenous and isolipidic experimental diets: fish‐meal‐based diet (FM); FM with 40% fish meal protein replaced by soybean meal protein (SBM); SBM+1% arginine (ARG1) and SBM+2% arginine (ARG2). Turbot‐fed SBM showed typical soybean meal‐induced enteropathy, characterized by an increase in the thickness of lamina propria, as well as significant decreases in the absorptive surface and activities of intestinal brush border membrane enzymes and Na+, K+‐ATPase. On the contrary, fish‐fed ARG1 showed enhanced intestinal mucosal barrier function in terms of the enhanced gene expression of anti‐inflammatory cytokine and barrier‐forming tight junction proteins, as well as depressed gene expression of pro‐inflammatory cytokines and pore‐forming tight junction proteins. Fish‐fed AGR2 showed intermediate intestinal performances between SBM and AGR1. Dietary arginine (1%) also significantly regulated the expression of AMP‐activated protein kinase α1 (AMPKα1), myosin light chain kinase (MLCK) and nuclear transcription factor‐κB p65 (NF‐κB p65), and these regulations correlated well with its regulations on intestinal mucosal barrier related genes at all sampling time‐points. In conclusion, arginine supplementation (1%) in diet for turbot mitigated the soybean meal‐induced enteropathy by enhancing the intestinal mucosal barrier function. The activation of AMPKα1 signalling molecule as well as the suppression of NF‐κB p65 and MLCK signalling molecules may mediate the beneficial effects of arginine.

No abstract

Soybean meal-induced enteropathy (SBMIE) is prevalent in aquaculture. The aim of this study is to evaluate the role of daidzein on SBMIE of juvenile turbot (Scophthalmus maximus L.) by feeding with fish meal diet (FM), soybean meal diet (SBM, 40% fish meal protein in FM replaced by soybean meal protein) and daidzein diet (DAID, 40 mg/kg daidzein supplemented to SBM) for 12 weeks. We found that daidzein supplementation elevated the gene expression of anti-inflammatory cytokine TGF-β, decreased gene expression of pro-inflammatory cytokines TNF-α and signal molecules p38, JNK and NF-κB. SBM up-regulated the genes expression related to oxidative stress and apoptosis, but dietary daidzein restored it to the similar level with that in FM group. Moreover, dietary daidzein up-regulated gene expression of tight junction protein, and modified the intestinal microbial profiles with boosted relative abundance of phylum Proteobacteria and Deinococcus–Thermus, genera Sphingomonas and Thermus, species Lactococcus lactis, and decreased abundance of some potential pathogenic bacteria. In conclusion, dietary daidzein could ameliorate SBM-induced intestinal inflammatory response, oxidative stress, mucosal barrier injury and microbiota community disorder of turbot. Moreover, p38, JNK and NF-κB signaling might be involved in the anti-inflammatory process of daidzein, and daidzein itself might act as an antioxidant to resist SBM-induced oxidative damage.

As the significance of the gut microbiota has become increasingly realized, a large number of related studies have emerged. With respect to the gut microbial composition of fish, the predominant gut microbes and core gut microbiota have been reported by many researchers. Our understanding of fish gut microbiota, especially its functional roles, has fallen far behind that of terrestrial vertebrates, although previous studies using gnotobiotic zebrafish models have revealed that the gut microbiota performs a significant role in gut development, nutrient metabolism and immune responses. Given that environmental factors of marine habitats are very different from those of freshwater habitats, a distinct difference may exist in the gut microbiota between freshwater and marine fish. Therefore, this review aims to address the advances in marine fish gut microbiota in terms of methodologies, the gut microbial composition, and gnotobiotic models of marine fish, the important factors (host genotype and three environmental factors: temperature, salinity and diet) that drive marine fish gut microbiota, and significant roles of the gut microbiota in marine fish.

A 74‐day feeding trial was conducted to evaluate the effects of dietary astaxanthin (ASTX) on antioxidative status, inflammatory response and microbiota in the intestine of tiger puffer. Four diets differed only in ASTX content, that is, 0 (Control), 50 (ASTX50), 100 (ASTX100) and 500 (ASTX500) mg/kg. Compared with Control, ASTX50 and ASTX100 significantly reduced the malondialdehyde content and spared the activities of antioxidative enzymes in hindgut; however, ASTX500 had higher activity and gene expression of antioxidative enzymes. Nuclear factor‐erythroid 2 p45‐related factor 2 (Nrf2) and Kelch‐like ECH‐associated protein 1 (Keap1) signalling were probably involved in the transcriptional regulation of antioxidative enzymes by dietary ASTX. Compared with Control and ASTX500, ASTX50 and ASTX100 decreased the leucocyte infiltration in the lamina propria of hindgut and down‐regulated the gene expression of tumour necrosis factor‐α (TNF‐α) and interleukin‐8 (IL‐8). ASTX markedly affected the overall structure of intestinal microbiota. The relative abundance of Arcobacter, which has harmful properties, was the lowest in ASTX100 but the highest in ASTX500. In conclusion, dietary ASTX at 50 or 100 mg/kg improved the antioxidative status, alleviated the inflammation and favourably modulated the microbiota in tiger puffer intestine, but excess ASTX exerted contrary effects.