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A 30-day feeding trial was conducted to investigate the effects of the supplementation of mannan oligosaccharide (MOS) in the diet on the skin wound healing process of juvenile turbot (Scophthalmus maximus). Two groups of diets were formulated, the control diet (CON) and the control diet supplemented with 0.16 % MOS (MOS), which were fed to the turbot separately. Each group had 3 replicates, with 20 fish per replicate. At the end of the feeding trial, all the fish were weighed and counted. Then four fish per tank were randomly selected for sampling, and the skin of the rest fish was wounded by a biopsy punch. The wounded fish continued to be fed as usual with the same diets respectively, and then sampled again at the 1, 3, and 7 day(s) post wounding (dpw). The results by image analysis showed that the wound closure rate of wounded fish was significantly improved by the supplementation of dietary MOS. As for the results of gene expression, dietary MOS promoted the expression of pro-inflammatory factors (il-1β & tnf-α) and decreased the expression of anti-inflammatory factors (tgf-β1 & il-10). It also enhanced the expression of genes related to re-epithelialization (mmp-9, fgf2, tgf-β1, rock1), as well as new tissue formation and remodeling (fn1, lamb2, col1-α, vegf). Furthermore, dietary MOS promoted re-epithelialization, cell proliferation, collagen deposition, and angiogenesis according to the histomorphological observation. In addition, the supplementation of MOS modified the communities of skin microbiota, decreasing the abundance of Rolstonia, Pseudomonas, and Aeromonas, while increasing the abundance of Pseudoalteromonas luteoviolacea and Shewanella colwellianav. In conclusion, the supplementation of dietary MOS (0.16 %) can promote the re-epithelialization and the recruitment of inflammatory cells, stimulate ECM biosynthesis and angiogenesis, modify the communities of skin microbiota, and ultimately promote the skin wound healing process., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Fish physiological health is often negatively impacted by high-temperature environments and there are few studies on how dietary lipids affect fish growth and physiology when exposed to heat stress. The main objective of this research was to examine the impact of dietary lipid levels on growth and physiological status of juvenile turbot (Scophthalmus maximus L.) and determine if dietary lipid concentration could alleviate the possible adverse effects of heat stress. Five diets containing 6.81%, 9.35%, 12.03%, 14.74%, and 17.08% lipid, respectively, were formulated and fed to turbot (initial weight 5.13 ± 0.02 g) under high-temperature conditions (24.0-25.0 °C). Meanwhile, the diet with 12.03% lipid (considered by prior work to be an optimal dietary lipid level) was fed to turbot of the same size at normal temperature. Results suggested that, among the different dietary lipid levels under high-temperature conditions, fish fed the optimal lipid (12.03%) exhibited better growth compared to non-optimal lipid groups, as evidenced by higher weight gain and specific growth rate. Simultaneously, the optimal lipid diet may better maintain lipid homeostasis, as attested by lower liver and serum lipid, along with higher liver mRNA levels of lipolysis-related genes (pgc1α, lipin1, pparα, lpl and hl) and lower levels of synthesis-related genes (lxr, fas, scd1, pparγ, dgat1 and dgat2). Also, the optimal lipid diet might mitigate oxidative damage by improving antioxidant enzyme activity, decreasing malondialdehyde levels, and up-regulating oxidation-related genes (sod1, sod2, cat, gpx and ho-1). Furthermore, the optimal lipid may enhance fish immunity, as suggested by the decrease in serum glutamic-oxalacetic/pyruvic transaminase activities, down-regulation of pro-inflammatory genes and up-regulation of anti-inflammation genes. Correspondingly, the optimal lipid level suppressed MAPK signaling pathway via decreased phosphorylation levels of p38, JNK and ERK proteins in liver. In summary, the optimal dietary lipid level facilitated better growth and physiological status in turbot under thermal stress., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023. Published by Elsevier Inc.)

An 8-week growth trial was performed to investigate the protective effects of methanotroph bacteria meal (MBM) produced from methane against soybean meal-induced enteritis (SBMIE) in juvenile turbot (Scophthalmus maximus L.). Five isonitrogenous and isolipidic diets were formulated: fishmeal-based diet (FM, the control group); FM with approximate 50% of fishmeal substituted by 399.4 g/kg soybean meal (SBM); SBM supplemented with 63.6, 127.2 and 190.8 g/kg MBM (named MBM1, MBM2 and MBM3), each diet was randomly assigned to triplicate fibreglass tanks. Results showed that fish fed with SBM exhibited enteritis, identified by reduced relative weight of intestine (RWI), as well as expanded lamina propria width and up-regulated gene expression of pro-inflammatory cytokines (tnf-α, il-6 and il-8) in intestine. While the above symptoms were reversed when diet SBM supplemented with MBM at the levels of 63.6 and 127.2 g/kg, as well as characterized by up-regulated gene expression of anti-inflammatory cytokines (tgf-β and il-10) and tight junction protein (claudin3, claudin4 and claudin7) in intestine. Intestinal transcriptome analysis showed that the differentially expressed genes between groups FM and SBM predominantly enriched in the JAK-STAT signaling pathway, and the enrichment of differentially expressed genes between groups SBM and SBM supplemented with 63.6 g/kg MBM was in the inflammatory bowel disease (IBD) and JAK-STAT signaling pathway. To be specific, the expression of jak1, jak2b, stat1 and stat5a was significantly up-regulated when fish fed with SBM, suggested the activation of JAK-STAT signaling pathway, while the expression of these above genes was depressed by providing MBM to diet SBM, and the gene expression of toll-like receptors tlr2 and tlr5b showed a similar pattern. Moreover, intestinal flora analysis showed that community richness and abundance of beneficial bacteria (Cetobacterium and acillus_coagulans) were improved when fish fed with SBM supplemented with 63.6 g/kg MBM. Overall, methanotroph bacteria meal may alleviate SBMIE by regulating the expression of tight junction protein, toll-like receptors and JAK-STAT signaling pathway, as well as improving intestinal flora profile, which would be beneficial for enhancing the immune tolerance and utilization efficiency of turbot to dietary soybean meal., Competing Interests: Declaration of competing interest The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024. Published by Elsevier Ltd.)

As one of short-chain fatty acids, butyrate is an important metabolite of dietary fiber by the fermentation of gut commensals. Our recent study uncovered that butyrate promoted IL-22 production in fish macrophages to augment the host defense. In the current study, we further explored the underlying signaling pathways in butyrate-induced IL-22 production in fish macrophages. Our results showed that butyrate augmented the IL-22 expression in head kidney macrophages (HKMs) of turbot through binding to G-protein receptor 41 (GPR41) and GPR43. Moreover, histone deacetylase 3 (HDAC3) inhibition apparently up-regulated the butyrate-enhanced IL-22 generation, indicating HDACs were engaged in butyrate-regulated IL-22 secretion. In addition, butyrate triggered the STAT3/HIF-1α signaling to elevate the IL-22 expression in HKMs. Importantly, the evidence in vitro and in vivo was provided that butyrate activated autophagy in fish macrophages via IL-22 signaling, which contributing to the elimination of invading bacteria. In conclusion, we clarified in the current study that butyrate induced STAT3/HIF-1α/IL-22 signaling pathway via GPCR binding and HDAC3 inhibition in fish macrophages to activate autophagy that was involved in pathogen clearance in fish macrophages., Competing Interests: Conflict of interest disclosure The authors have no relevant financial or non-financial interests to disclose., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

It has been known that vitamin D 3 (VD 3 ) not only plays an important role in regulating calcium and phosphorus metabolism in animals, but also has extensive effects on immune functions. In this study, the mechanism how VD 3 influences bactericidal ability in turbot was explored. The transcriptomic analysis identified that dietary VD 3 significantly upregulated the gene expression of C-type lectin receptors (CLRs), including mannose receptors (mrc1, mrc2, pla2r1) and collectins (collectin 11 and collectin 12) in turbot intestine. Further results obtained from in vitro experiments confirmed that the gene expression of mannose receptors and collectins in head-kidney macrophages (HKMs) of turbot was induced after the cells were incubated with different concentrations of VD 3 (0, 1, 10 nM) or 1,25(OH) 2 D 3 (0, 10, 100 pM). Meanwhile, both phagocytosis and bactericidal functions of HKMs were significantly improved in VD 3 or 1,25(OH) 2 D 3 -incubated HKMs. Furthermore, phagocytosis and bacterial killing of HKMs decreased after collectin 11 was knocked down. Moreover, VD 3 -enhanced antibacterial activities diminished in collectin 11-interfered cells. Interestingly, the evidence was provided in the present study that inactive VD 3 could be metabolized into active 1,25(OH) 2 D 3 via hydroxylases encoded by cyp27a1 and cyp27b1 in fish macrophages. In conclusion, VD 3 could be metabolized to 1,25(OH) 2 D 3 in HKMs, which promoted the expression of CLRs in macrophages, leading to enhanced bacterial clearance., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Vitamin D (VD) plays a vital role in various physiological processes in addition to its classic functions on maintaining the balance of Ca and P metabolism. However, there still are gaps to understand in depth the issues on the precise requirement, metabolic processes and physiological functions of VD in fish. In this study, we investigated the effects of VD on the growth, intestinal health, host immunity and metabolism in turbot ( Scophthalmus maximus L.), one important commercial carnivorous fish in aquaculture, through the supplementation of different doses of dietary VD 3 (0, 200, 400, 800 and 1600 μg VD 3 /kg diet). According to our results, the optimal VD 3 level in the feed for turbot growth was estimated to be around 400 IU/kg, whereas VD 3 deficiency or overdose in diets induced the intestinal inflammation, lowered the diversity of gut microbiota and impaired the host resistance to bacterial infection in turbot. Moreover, the level of 1 α ,25(OH) 2 D 3 , the active metabolite of VD 3 , reached a peak value in the turbot serum in the 400 μg group, although the concentrations of Ca and phosphate in the turbot were stable in all groups. Finally, the deficiency of dietary VD 3 disturbed the nutritional metabolism in turbot, especially the metabolism of lipids and glucose. In conclusion, this study evaluated the optimal dose of dietary VD 3 for turbot and provided the evidence that VD has a significant impact on intestinal health, host immunity and nutritional metabolism in fish, which deepened our understanding on the physiological functions and metabolism of VD 3 in fish.

Vitamin D 3 (VD 3 ) participated widely in the nuclear factor-κB (NF-κB)-mediated inflammation, apoptosis, and autophagy through the vitamin D receptor (VDR). However, the molecular mechanisms remain not understood in teleost. The present study investigated the functions of VD 3 /VDR on intestinal inflammation, autophagy, and apoptosis of turbot in vivo and in vitro . Triple replicates of 30 fish were fed with each of three diets with graded levels of 32.0 (D 0 ), 1012.6 (D 1 ), and 3978.2 (D 2 ) IU/kg VD 3 . Obvious intestinal enteritis was observed in the D 0 group and followed with dysfunction of intestinal mucosal barriers. The intestinal inflammatory response induced by VD 3 deficiency was regulated by the NF-κB/inflammasome signalling. The promotion of intestinal apoptosis and suppression of intestinal autophagy were also observed in the D 0 group. Similarly, VD 3 deficiency in vitro induced more intense inflammation regulated by NF-κB/inflammasome signalling. The mutually exclusive apoptosis and autophagy were also observed in the group without 1,25(OH) 2 D 3 in vitro , accompanied by similar changes in apoptosis and autophagy increased apoptosis. The gene expression of VDRs was significantly increased with the increasing VD 3 supplementation both in vivo and in vitro . Moreover, VDR knockdown in turbot resulted in intestinal inflammation, and this process relied on the activation of inflammasome mediated by NF-κB signalling. Simultaneously, intestinal apoptosis was promoted, whereas intestinal autophagy was inhibited. In conclusion, VD 3 deficiency could induce intestinal inflammation via activation of the NF-κB/inflammasome pathway, intestinal apoptosis, and autophagy formed a mutually exclusive relation in teleost. And VDR is the critical molecule in those processes., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer SZ declared a shared affiliation with authors GL and JD to the editor at the time of review., (Copyright © 2022 Chen, Huang, Yongyut, Li, Esteban, Jintasataporn, Deng, Zhang, Ai, Mai and Zhang.)

Accumulating evidence supports that vitamin D 3 (VD 3 ) possesses immunomodulatory properties besides its classical actions in calcium and bone homeostasis. In this study, juvenile turbots were fed with the diets containing 0 IU/kg VD 3 or the optimum dose of 400 IU/kg VD 3 for 8 weeks. To investigate the effects of VD 3 on anti-infectious immunity in fish, 10 7  CFU Edwardsiella tarda was injected intraperitoneally to each juvenile turbot after the feeding trial. Our results showed that the mortality of infected turbots with dietary VD 3 was much lower than that in VD 3 deficient group, and the supplementation of dietary VD 3 significantly reduced the bacterial load in the spleen of infected turbots. Further analysis demonstrated that the production of reactive oxygen species (ROS) in haemocytes and lysozyme activity in serum was elevated, and the responses of T cells and B cells were modulated in VD 3 -supplemented turbots. Moreover, the inflammation was significantly exacerbated in the infected turbots fed with 0 IU/kg VD 3 compared to the fish fed with 400 IU/kg VD 3 . In addition, the head kidney macrophages (HKMs) in turbots were isolated and incubated with VD 3 in vitro, the results showed that VD 3 significantly promoted the bactericidal activity in HKMs. In conclusion, our study has shown clear evidence that VD 3 positively regulates the innate and adaptive immunity in fish, which is beneficial to the defense in fish against pathogen infection., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

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.

Cecropin AD (CAD) is a commercial cationic antimicrobial peptide that has been seldom studied in marine fish. This study investigated the effects of dietary CAD on intestinal health, immune response, disease resistance, and growth performance of turbot. A diet using fishmeal and plant protein as the main protein resources was used as the control (crude protein 53%, crude lipid 12%). CAD was supplemented into the control diet at the level of 250, 500, 750, and 1000 mg kg -1 to formulate four experimental diets, C1, C2, C3, and C4, respectively. No significant difference was observed in fish growth performance, feed utilization efficiency and whole-body composition among all groups. Dietary CAD significantly increased the activity of lysozyme and complement component 3 level in both serum and distal intestine (DI), as well as the immunoglobulin M content in DI. The gene expression of immune cytokines such as IFN-γ, IL-1β, and chemokine SmCCL19, and the goblet cell number in DI were also significantly increased by dietary CAD supplementation. Compared with the control group, the microbiota analysis indicated group C4 showed significantly decreased α-diversity, obvious alternation in dominant bacteria composition at phylum level, different clustering, and significantly decreased relative abundance of Lactobacillus. Besides, the relative abundance of Bacteroides was significantly decreased in groups C1, C3, and C4. In addition, the lowest mortality of turbot challenged with Edwardsiella tarda was observed in fish fed diets C2 and C3. In conclusion, moderate levels of CAD in diet of turbot improved the intestinal immune response without disrupting the intestinal bacterial community, and enhanced the disease resistance. However, dietary CAD at 1000 mg kg -1 greatly affected the intestinal bacterial composition and showed potentially inhibitory effects towards Lactobacillus., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

A 12-week feeding trial was conducted to investigate the effect of dietary daidzein on the intestinal mucosal barrier function and the intestinal microbiota profile of juvenile turbot (Scophthalmus maximus L.). Three isonitrogenous and isolipidic experimental diets were formulated to contain 0 (FM), 40 (D.40) and 400 (D.400) mg kg -1 daidzein, respectively. Fish fed D.400 had significantly lower growth performance than fish fed D.40. Dietary daidzein significantly increased the feed efficiency, while significantly decreased the feed intake. Daidzein supplementation increased the activity of total anti-oxidative capacity and the gene expression of anti-inflammatory cytokine transforming growth factor-β1, Mucin-2 and tight junction proteins (Tricellulin, Zonula occludens-1 transcript variant 1, Zonula occludens-1 transcript variant 2 and Claudin-like and Occludin), and down-regulated the gene expression of pro-inflammatory cytokines interleukin-1β and tumor necrosis factor-α in the intestine of turbot. Dietary daidzein increased intestinal microbial diversities, the abundance of several short chain fatty acids producers, and decreased the abundance of some potential pathogenic bacteria. However, D.400 had dual effects on lactic acid bacteria and increased the abundance of potential harmful bacterium Prevotella copri. Collectively, dietary daidzein at the levels of 40 and 400 mg kg -1 could enhance the intestinal mucosal barrier function and alter the intestinal microbiota of turbot. However, high dose of daidzein must be treated with caution for its unclear effects on intestinal microbiota of turbot in the present study., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

A 12-week feeding trial was conducted to investigate the effect of citric acid on the involvement of TLRs in the soybean meal induced inflammatory response and tight junction disruption in the distal intestine of juvenile turbot (Scophthalmus maximus L.). Four isonitrogenous and isolipidic practical diets were formulated: fish meal-based diet (FM); 40% fish meal protein in FM replaced with soybean meal protein (SBM); SBM + 1.5% citric acid and SBM + 3% citric acid. Compared to the FM, diet SBM significantly increased the gene expression of TLRs (TLR2, TLR3, TLR5b, TLR9, TLR21, TLR22) and MyD88, as well as TLR related molecules (NF-κB, IRF-3, p38 and JNK), which were remarkably reduced by dietary citric acid. Similarly, citric acid supplementation in SBM markedly depressed gene expression of pro-inflammatory cytokines (TNF-α and IFN-γ) and pore-forming tight junction protein Claudin-7, and enhanced gene expression of the anti-inflammatory cytokine TGF-β1 and TJ proteins related to the decrease in paracellular permeability (Claudin-3, Claudin-4, Occludin, Tricellulin and ZO-1). Compared to the SBM, the concentration of IgM and C4 in serum was significantly reduced by dietary citric acid. In brief, dietary citric acid could synchronously inhibit TLRs-dependent inflammatory response regulated by NF-κB and IRF3, as well as cause TLRs-dependent tight junction disruption modulated by p38 and JNK. Therefore, citric acid could function on mitigating soybean meal induced enteropathy in the distal intestine of juvenile turbot., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

A 12-week feeding trial was conducted to evaluate the effects of dietary sodium butyrate (NaBT) on the intestinal health of juvenile turbot (Scophthalmus maximus L.), in terms of inflammatory status, mucosal barriers and microbiota. Three isonitrogenous and isolipidic practical diets were used: (1) fish meal based group (FM); (2) soybean meal group (SBM), soy protein replacing 40% fish meal protein in FM; (3) NaBT group, 0.2% NaBT supplemented in SBM. Each diet was fed to triplicate tanks (30 fish in each tank). The current results showed that 0.2% dietary NaBT improved the growth performance of fish and alleviated the enteropathy, increasing the absorptive surface and mitigating the infiltration of mixed leukocytes in lamina propria. Fish fed the NaBT diet presented increased activities of intestinal brush border enzyme and similar nutrient digestibility with the FM group. Compared to SBM, the inclusion of 0.2% NaBT in diet significantly up-regulated the intestinal gene expression of tight junction proteins and down-regulated the gene expression of TNF-α and NF-κB. The gut microbial communities of the NaBT group were closer to the FM group than to the SBM group, in terms of PCoA, UPGMA and Heatmap analyses based on weighted Unifrac distance. The relative abundance of several dominant bacteria at the phylum (Proteobacteria, Bacteroidetes, Deinococcus-Thermus and Actinobacteria) and genus level (Thermus, Acinetobacter, Bacteroides and Silanimonas) were altered by dietary NaBT. In conclusion, dietary NaBT had positive roles in protecting the intestinal health of turbot from the impairment of soybean meal., (Copyright © 2019. Published by Elsevier Ltd.)

Turbot (Scophthalmus maximus) is an economically important fish that is farmed by aquaculture for human consumption. Aquacultured turbot are commonly fed a high-lipid diet; however, this diet causes excessive lipid deposition and the overexpression of pro-inflammatory cytokines. Studies in mammals have indicated that a relationship exists between pro-inflammatory cytokine overexpression and altered lipid metabolism through the activation of suppressor of cytokine signaling 3 (SOCS3). In this study, we investigated the relationship between SOCS3 and triglyceride (TG) deposition and mechanism of SOCS3 activation in farmed turbot fed high-lipid diet (HLD). TG content increased with SOCS3 production, mediated by toll-like receptor-nuclear transcription factor kappa-B (TLR-NFκB) signaling in the liver of turbot fed a HLD and in turbot primary liver cells incubated with oleic acid (OA). Overexpression of SOCS3 increased TG deposition via the increased production of mature sterol regulatory element binding protein 1 (m-SREBP-1). Knockdown of SOCS3 in turbot primary liver cells resulted in normalized TG deposition and decreased m-SREBP-1 production. These results suggest that the HLD and OA can induce cytokine expression by activating the TLR-NFκB signaling pathways, resulting in increased SOCS3 expression. It is proposed that SOCS3 enhances m-SREBP-1 production, leading to TG deposition. These findings provide important new insights into the relationship between cytokine expression and TG deposition and mechanism of HLD-induced pro-inflammatory response, which could help to improve the health of farmed turbot and a better understanding of fish immunity., (Copyright © 2017. Published by Elsevier Ltd.)

In this study, the mechanism that TNFα inhibits lipid deposition through GSK-3β/β-catenin signaling was investigated in the liver of juvenile turbot (Scophthalmus maximus L.) by injection of TNFα or TNFα inhibitor pomalidomide (POM). It was found that TNFα inhibited the expression of GSK-3β and induced β-catenin expression. TNFα inhibited the expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα), as well as the activity of lipoprotein lipase (LPL) and fatty acid synthetase (FAS). In addition, the level of triglyceride (TG), total cholesterol (TC), nonesterified fatty acid (NEFA), and glycerol was decreased by TNFα treatment in the liver. In the plasma, the level of TG, TC, low density lipoprotein cholesterol (LDL-C), NEFA, and glycerol was decreased, but high density lipoprotein cholesterol (HDL-C) was increased by TNFα treatment. However, compared to TNFα, POM had the opposite effect on the biochemical indexes and genes related to lipid deposition in the liver. The results indicated that TNFα may regulate hepatic lipid metabolism and fat distribution through GSK-3β/β-catenin signaling as well as transcription factors PPARγ and C/EBPα in juvenile turbot., (Copyright © 2015 Elsevier Inc. All rights reserved.)

In this study, the mechanism that Wnt/β-catenin signaling inhibits lipogenesis was investigated in the liver of juvenile turbot (Scophthalmus maximus L.) by LiCl or XAV939 treatment. Wnt/β-catenin signaling was activated by LiCl treatment or inhibited by XAV939 treatment through regulating the expression of glycogen synthase kinase-3β (GSK-3β) and Wnt10b. In addition, the expression of lipoprotein lipase (LPL), fatty acid synthetase (FAS), peroxisome proliferator-activated receptor γ (PPARγ), and CCAAT/enhancer binding protein α (C/EBPα) was inhibited by LiCl treatment, but induced by XAV939 treatment. In the plasma of juvenile turbot, the level of nonesterified fatty acid (NEFA), glycerol, triglyceride (TG), total cholesterol (TC), and low density lipoprotein cholesterol (LDL-C) was decreased by LiCl treatment, which was related to the decrease of the activity of LPL and FAS. Thus the inhibitory effect of Wnt/β-catenin signaling on lipogenesis was associated with the expression of key enzymes and transcriptional factors. Wnt/β-catenin signaling may participate in inhibiting lipogenesis by inhibiting the expression of PPARγ and C/EBPα in the liver of juvenile turbot., (Copyright © 2015 Elsevier Inc. All rights reserved.)

The present study was conducted to investigate the effects of dietary arachidonic acid (ARA) on growth performance, fatty acid composition and ARA metabolism-related gene expression in larval half-smooth tongue sole (Cynoglossus semilaevis). Larvae (35 d after hatching, 54 (SEM 1) mg) were fed diets with graded concentrations of ARA (0.01, 0.39, 0.70, 1.07, 1.42 and 2.86 % dry weight) five times per d to apparent satiation for 30 d. Results showed that increased dietary ARA concentration caused a significant non-linear rise to a plateau in survival rate, final body weight and thermal growth coefficient, and the maximum values occurred with the 1.42 % ARA treatment. As dietary ARA increased to 1.07 or 1.42 %, activities of trypsin, leucine aminopeptidase and alkaline phosphatase levels increased, but they decreased with higher ARA concentrations. The fatty acid composition of tongue sole larvae was almost well correlated with their dietary fatty acid profiles, and the EPA content of the larvae decreased with increasing dietary ARA. Meanwhile, the partial sequences of COX-1a (cyclo-oxygenase-1a), COX-1b (cyclo-oxygenase-1b), COX-2 (cyclo-oxygenase-2), 5-LOX (5-lipoxygenase) and CYP2J6-like (cytochrome P450 2J6-like) were also obtained. Both COX-2 and 5-LOX mRNA expression levels significantly increased to a plateau in an 'L'-shaped manner as dietary ARA increased to 1.07 or 1.42 %, but no significant differences were found in the gene expression of COX-1a, COX-1b or CYP2J6-like. These results suggest that 1.07-1.42 % dietary ARA was beneficial to the growth performance of larval tongue sole, and the regulation of dietary ARA on the growth performance of larvae was probably involved in altering the mRNA expression of COX-2 and 5-LOX.