Dietary gamma-aminobutyric acid ameliorates growth impairment and intestinal dysfunction in turbot (Scophthalmus maximus L.) fed a high soybean meal diet.

Over-substitution of fishmeal with soybean meal (SBM) commonly induces inferior growth and intestinal dysfunction in fish. This study aims to evaluate whether dietary gamma-aminobutyric acid (GABA) could ameliorate the adverse effects in turbot fed a high-SBM diet (HSD). Two hundred and seventy turbots were randomly divided into three treatment groups including turbots fed on a control diet (CNT, containing 60% fishmeal), an HSD (with 45% fishmeal protein replaced by SBM), and an HSD supplemented with GABA (160 mg kg-1) for 53 days. The growth and feed utilization parameters were calculated and the intestinal antioxidant status, inflammation, apoptosis, and microbiota were evaluated using assay kits, histological analysis, qRT-PCR, high throughput sequencing, and bioinformatics analysis. The results showed that GABA ameliorated HSD-induced growth impairment and enhanced feed intake of turbot. GABA ameliorated HSD-induced intestinal oxidative stress and apoptosis by restoring the MDA content, CAT and T-AOC activities, and apoptosis-related gene (Bcl-2, Bax, Bid, and Caspase-3) expressions to similar levels to those in the CNT group. GABA also alleviated HSD-induced intestinal inflammation through down-regulating the expressions of TNF-α, IL-1ß, and NF-κB p65 and up-regulating the expression of TGF-ß1. Furthermore, GABA reversed HSD-induced microbiota dysbiosis through regulating the overall bacterial richness and dominative bacterial population. Spearman's correlation analysis indicated that the altered microbiota was closely associated with growth and intestinal function. Collectively, GABA could ameliorate HSD-induced intestinal dysfunction via relieving oxidative stress, inflammation, apoptosis and microbiota dysbiosis, and these findings would contribute to a better understanding of the function of GABA in the fish intestine.

Administration of commensal Shewanella sp. MR-7 ameliorates lipopolysaccharide-induced intestine dysfunction in turbot (Scophthalmus maximus L.).

This study was designed to evaluate whether the administration of commensal Shewanella sp. MR-7 (MR-7) could ameliorate lipopolysaccharide (LPS)-induced intestine dysfunction in turbot. Fish (body weight: 70.00 ± 2.00 g) were randomly divided into three groups including the control group treated with dough, the LPS group treated with dough plus LPS, and the LPS+MR-7 (LMR) group treated with dough plus LPS and MR-7. These three groups with 24 fish each were force-fed with 1 g dough daily for 7 continuous days. The results revealed that MR-7 administration ameliorated LPS-induced intestinal injury, showing higher intestinal villus and microvillus height. Further results showed that MR-7 could inhibit LPS-induced activation of TLR-NF-κB signaling thus maintaining the normal expression levels of cytokines and finally ameliorate the intestinal inflammatory response in turbot. Compared with the LPS group, LMR group had less goblet cells and lower mucin-2 expression level. Moreover, MR-7 restored LPS-induced down-regulation of tight junction protein-related gene expression (zonula occluden-1, occludin, tricellulin and claudin-3). Further investigations indicated that MR-7 partially counteracted LPS-induced changes in gut microbiota composition, enhanced the beneficial bacteria Lactobacillus and reduced the Pseudomonas, thus maintaining the overall microbiota balance. Taken together, the administration of MR-7 could effectively restore LPS-induced intestine function disorder in turbot by ameliorating inflammatory response, mucosal barrier dysfunction and microbiota dysbiosis.

Effects of dietary raw or Enterococcus faecium fermented soybean meal on growth, antioxidant status, intestinal microbiota, morphology, and inflammatory responses in turbot (Scophthalmus maximus L.).

Fermentation has been reported to improve the utilization of plant ingredients including soybean meal (SBM) by fish, but the detailed mechanism is still poorly understood. This study compared the effects of partial replacement of fish meal (FM) protein with SBM or Enterococcus faecium fermented SBM (EFSM) on the growth, antioxidant status, intestinal microbiota, morphology, and inflammatory responses in turbot (Scophthalmus maximus L.). The FM-based diet was used as the control (CONT). Two experimental diets were formulated in which 45% of the FM protein was replaced with SBM or EFSM. Each diet was fed to triplicate groups of fish (7.57 ± 0.01 g) twice daily for 79 d. Inferior growth performance was observed in SBM group, however, no significant depression was observed in EFSM group compared to the CONT group. The CONT group had the highest values of lysozyme, complement component 3, total antioxidant capacity, superoxide dismutase and catalase, followed by the EFSM group, and the lowest in SBM group. The malondialdehyde content was lowest in the CONT group, followed by the EFSM group, and was highest in the SBM group. Gut morphology showed that SBM diet induced alterations typical for intestinal inflammation including decreased villus and microvillus height, and increased width and inflammatory cell infiltration of the lamina propria. However, the EFSM group alleviated such SBM-induced intestinal pathological disruption. Paralleled with the morphological symptoms, the inflammatory gene expression levels of tumor necrosis factor alpha, interleukin-1 beta and interleukin-8 were highest in the SBM group, followed by the EFSM group, and were lowest in the CONT group. Furthermore, the intestinal microbiota analysis revealed that EFSM group had an overall more similar microbiota with CONT group than SBM group. Specifically, compared with the SBM group, EFSM group significantly enhanced the probiotics Lactobacillus and anti-inflammatory bacterium Faecalibaculum, and inhibited the Vibrio. Collectively, this study indicated that Enterococcus faecium fermentation effectively counteracted the negative effects of SBM by enhancing antioxidant capacity, suppressing inflammatory responses, and modulating gut microbiota in turbot.