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The trial was conducted to investigate the effects of the replacement of dietary fishmeal (FM) by the blend of Tenebrio molitor meal (TMM), Chlorella meal (CM), Clostridium autoethanogenum protein (CAP), cottonseed protein concentrate (CPC) on growth, protein utilization and intestinal health of gibel carp (Carassius gibelio, CAS Ⅴ). The FM-based diet was used as the control, and the blended proteins (TMM: CM: CAP: CPC) at ratios of 1 : 1:8 : 2 (BLEND A), 1 : 1:6 : 4 (BLEND B), and 1 : 1:4 : 6 (BLEND C) were used to replace FM at three levels (33%, 67%, 100%), respectively. The results showed that, compared to the control group, growth performance increased significantly when dietary FM was fully replaced by BLEND B (P < 0.05), while decreased by BLEND A (P < 0.05). The complete substitution of FM with BLEND B significantly upregulated the mRNA expression of intestinal proinflammatory cytokines, anti-inflammatory cytokines, and tight junction-related genes (P < 0.05), improving intestinal tissue morphology and health. And it also significantly increased intestinal trypsin activity (P < 0.05), upregulated the mRNA expression of amino acid sensory receptor-related and amino acid or peptide transport-related genes (P < 0.05), increased protein apparent digestibility coefficient (P < 0.05). The 100% substitution of FM with BLEND A significantly upregulated the mRNA expression of intestinal proinflammatory cytokines and downregulated the mRNA expression of anti-inflammatory cytokine il-10 (P < 0.05), reduced intestinal villus height (P < 0.05), and decreased protein apparent digestibility coefficient (P < 0.05). In conclusion, BLEND B could completely substitute dietary FM and was beneficial to the growth and health of gibel carp. Dietary digestible essential amino acids index (DEEAI) was found as an important indicator and should be higher than 79.5% to meet the maximum growth of fish. [ABSTRACT FROM AUTHOR]

The present study investigated the sequential regulation signals of high-carbohydrate diet (HCD)-induced hepatic lipid deposition in gibel carp (Carassius gibelio). Two isonitrogenous and isolipidic diets, containing 25% (normal carbohydrate diet, NCD) and 45% (HCD) corn starch, were formulated to feed gibel carp (14.82 ± 0.04 g) for 8 weeks. The experimental fish were sampled at 2nd, 4th, 6th, and 8th week. In HCD group, the hyperlipidemia and significant hepatic lipid deposition (oil red O area and triglyceride content) was found at 4th, 6th, and 8th week, while the significant hyperglycemia was found at 2nd, 4th, and 8th week, compared to NCD group (P < 0.05). HCD induced hepatic lipid deposition via increased hepatic lipogenesis (acc, fasn, and acly) but not decreased hepatic lipolysis (hsl and cpt1a). When compared with NCD group, HCD significantly elevated the hepatic sterol regulatory element binding proteins 1 (SREBP1) signals (positive hepatocytes and fluorescence intensity) at 4th, 6th, and 8th week (P < 0.05). The hepatic SREBP1 signals increased from 2nd to 6th week, but decreased at 8th week due to substantiated insulin resistance (plasma insulin levels, plasma glucose levels, and P-AKTSer473 levels) in HCD group. Importantly, the hepatic carbohydrate response element binding protein (ChREBP) signals (positive hepatocytes, fluorescence intensity, and expression levels) were all significantly elevated by HCD-induced glucose-6-phosphate (G6P) accumulation at 2nd, 4th, 6th, and 8th week (P < 0.05). Compared to 2nd and 4th week, the hepatic ChREBP signals and G6P contents was significantly increased by HCD at 6th and 8th week (P < 0.05). The HCD-induced G6P accumulation was caused by the significantly increased expression of hepatic gck, pklr, and glut2 (P < 0.05) but not 6pfk at 4th, 6th, and 8th week, compared to NCD group. These results suggested that the HCD-induced hepatic lipid deposition was mainly promoted by SREBP1 in earlier stage and by ChREBP in later stage for gibel carp. This study revealed the sequential regulation pathways of the conversion from feed carbohydrate to body lipid in fish. [ABSTRACT FROM AUTHOR]

This study investigated the potential role of curcumin (CUR) in preventing oxidative stress and ferroptosis induced by ammonia exposure in gibel carp. Experimental fish (initial weight: 11.22 ± 0.10 g, n = 150) were fed diets supplemented with or without 0.5% CUR for 56 days, followed by a 24 h ammonia (32.5 mg/L) exposure. Liver damages (aspartate aminotransferase (AST), alanine aminotransferase (ALT), adenosine deaminase (ADA), and alkaline phosphatase (ALP)) and oxidative stress enzyme activities (reactive oxygen species (ROS), malondialdehyde (MDA); and the content of antioxidant capacity (T-AOC), superoxide dismutase (SOD), and glutathione peroxidase (GPx)) were induced by ammonia stress. The antioxidant capacity was decreased, as indicated by inhibited gene expression of nuclear factor erythroid 2-related factor 2 (nrf2), heme oxygenase-1 (ho-1), catalase (cat), and sod. Ferroptosis was induced by ammonia stress, as suggested by upregulated mRNA levels of nuclear receptor coactivator 4 (ncoa4), transferrin receptor 1 (tfr1), and iron-responsive element-binding protein 2 (ireb2), and downregulated expression of glutathione peroxidase 4 (gpx4), ferroportin (fpn), and ferritin heavy chain 1 (fth1). In addition, both mRNA and protein levels of ferroptosis markers acyl-CoA synthetase long-chain family member 4 (ACSL4) and prostaglandin-endoperoxide synthase 2 (PTGS2) were upregulated, while cystine/glutamate antiporter (SLC7A11) was downregulated. However, liver injury and ferroptosis in fish induced by ammonia could be attenuated by CUR. Collectively, these findings demonstrate that CUR ameliorates oxidative stress and attenuates ammonia stress-induced ferroptosis. This study provides a new perspective on potential preventive strategies against ammonia stress in gibel carp by dietary CUR. [ABSTRACT FROM AUTHOR]

Our previous studies in gibel carp (Carassius gibelio) have shown that cadmium (Cd) exposure elicits deleterious effects depending on the genetic background, and thus we hypothesized that mitigation via nutritional intervention may vary between strains. Therefore, two gibel carp strains (the A and F strains) were fed diets supplemented with 0% or 1% taurine for 8 weeks prior to 96 h Cd exposure, and the responses of antioxidant pathways, endoplasmic reticulum (ER) stress, autophagy, and apoptosis were investigated. The results showed that taurine supplementation had no effect on the growth performance of gibel carp. After Cd exposure, histological damage to mitochondria and ER, induction of oxidative stress and antioxidant responses, occurrence of ER stress, and apoptotic signals were observed in the livers. Upon the diet effects, taurine supplementation alleviated the ER-stress-induced autophagy and apoptosis after Cd exposure and stimulated antioxidant pathways. Regarding the difference between strains, taurine played a protective role in alleviating Cd toxicity through the antioxidant response, ER stress, and autophagy in the F strain, whereas such effects were achieved by the attenuation of apoptosis in the A strain. Taken together, our results demonstrate the potential use of taurine in the mitigation of heavy metal toxicity in aquatic organisms. [ABSTRACT FROM AUTHOR]

An 8-week feeding trial was conducted to investigate carbohydrate use in a low-lipid diet between different strains of gibel carp (Carassius gibelio). The wild-type Dongting strain and artificially selected CASIII strain were fed three levels of carbohydrate: 15%, 30%, and 45%, in a low-lipid formulation (4%). The results showed that low-lipid supplementation with high carbohydrate seems to improve the feeding rate (FR) and specific growth rate (SGR), while it did not result in hyperglycaemia in gibel carp. Transcriptional regulation was slightly affected by carbohydrate levels; only hepatic pfk expression was more increased in the 30% and 45% carbohydrate diets than in the 15% carbohydrate diet (p < 0.05). Regarding the strains, CASIII obtained higher growth performance by having higher FR and SGR than Dongting (p < 0.05). Relatively higher glycaemia was found in CASIII, and it was coupled with increased plasma triglycerides and insulin (p > 0.05). Enhanced gene expression of pk involved in glycolysis and decreased mRNA levels of pepck in gluconeogenesis were also observed in CASIII (p < 0.05). There were strong strain ∗ diet interactions of gene expression involved in lipogenesis, and Dongting had higher mRNA levels of srebp-1, acly, and fas when fed carbohydrate at 45% (p < 0.05). In conclusion, the tolerant level of carbohydrates in a low-lipid diet could be up to 45% for gibel carp by an improvement of growth and noninducement of postprandial plasma glucose. CASIII had a better ability to use dietary carbohydrates for growth with active glycolysis and restrained gluconeogenesis, and Dongting had more potential in lipid metabolism in response to carbohydrate intake. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Normally, fish will decrease food intake or even stop feeding during the winter. In previous studies, two widely cultured gibel carp strains (strain A and strain F) showed differences in lipid and glucose metabolism. Therefore, we hypothesized that the physiological changes during the overwintering period would be different between the two strains. Thus, the two strains were starved for 77 days, after which the levels of glucose and lipid metabolism, ER stress, autophagy, and apoptosis were determined. The starvation increased hepatic glycogenolysis and fatty acid β-oxidation but suppressed lipogenesis in both strains overwintering. Considering the effects of genotype, strain F had higher levels of ER stress and autophagy but lower levels of apoptosis than strain A, suggesting that strain F might be more resistant to overwintering starvation. The interactions between strains and starvation periods were observed in plasma triglyceride contents and the mRNA levels of pyruvate kinase (pk), sterol regulatory element binding protein 1 (srebp1), activating transcription factor 4 (atf4), and autophagy protein 12 (atg12). In conclusion, long-term starvation during winter could induce hepatic glycogenolysis and fatty acid β-oxidation but suppress lipogenesis, ER stress, autophagy, and apoptosis in gibel carp, and strain F may be more resistant to starvation during winter. Taken together, these results discovered the responses to prolonged starvation stress during winter in two strains of gibel carp and could provide information for genotype selection, especially for selecting strains better adapted to winter. [ABSTRACT FROM AUTHOR]

Gelatin and carboxymethyl cellulose (CMC) were often used as binders due to their binding ability. To investigate the effects of gelatin and CMC supplementation on feed quality, intestinal ultrastructure and growth performance of gibel carp, six pelleted feed were formulated: control; supplemented with gelatin (10 g/kg, 30 g/kg and 50 g/kg); and supplemented with CMC (10 g/kg and 30 g/kg). Increased gelatin supplementation levels reduced feed solubility and pellet softening (p <.05) and decreased chemical oxygen demand in the surrounding water after pellets were immersed (p <.05). Increased levels of gelatin supplementation enhanced digesta viscosity and reduced intestinal microvilli length and digestive enzymes activities (chymotrypsin and amylase; p <.05) of fish. Fish‐fed diets supplemented with 30 g/kg gelatin had higher levels of plasma total free amino acids and glucose (p <.05) than fish fed 10 g/kg and 50 g/kg gelatin. Feed supplemented with 10 g/kg CMC were softer than those supplemented with 30 g/kg CMC (p <.05); fish‐fed diets supplemented with 10 g/kg CMC had longer intestinal microvilli (p <.05) than fish fed 30 g/kg CMC. Thus, our results indicated that either gelatin or CMC is applicable to supplement in the feed for improving feed quality and without negative effect on growth performance of gibel carp. [ABSTRACT FROM AUTHOR]

Ammonia is recognized as an environmental stressor for fish. As resveratrol (RES) has anti-inflammatory and antioxidant properties, we hypothesized that RES could attenuate the response to ammonia exposure in gibel carp. Therefore, gibel carp were fed a diet containing RES for eight weeks, followed by acute ammonia stimulation. Stress induced by acute ammonia exposure could be ameliorated by RES, manifested by down-regulated plasma glucose, and up-regulated C3 and IgM levels. Furthermore, decreased AST and LDH; enhanced T-AOC, SOD, and GPx in the liver; and reduced damage to gill and liver tissues indicated that RES attenuated oxidative and tissue damage induced by ammonia exposure. Moreover, RES activated the Nrf2/HO-1 pathway and up-regulated the expression of several antioxidant genes. RES enhanced anti-inflammatory activity as reflected by activation of the NF-κB pathway, down-regulated the expression of pro-inflammatory cytokines (nfκb , tnf-α , and il-1β), and up-regulated the expression of anti-inflammatory cytokines (il-4 and il-10). In terms of mitochondrial function, RES up-regulated protein levels of p-AMPK, SIRT1, and PGC-1α; inhibited mitochondrial fission; promoted mitochondrial fusion and biogenesis-related gene expression. Overall, the results suggest that RES mediated the Nrf2/HO-1, NF-κB, and AMPK/SIRT1/PGC-1α pathways to attenuate oxidative stress, inflammation, and mitochondrial dysfunction induced by ammonia in gibel carp. [Display omitted] • Acute ammonia exposure induced severe tissue damage and exacerbated oxidative stress in gibel carp. • Acute ammonia exposure up-regulated the expression of pro-inflammatory mediators, leading to an inflammatory response. • Acute ammonia exposure inhibited mitochondrial fusion and biogenesis, and ultimately led to mitochondrial dysfunction. • RES effectively attenuated pathologies by acting on the Nrf2/HO-1, NF-κB, and AMPK/SIRT1/PGC-1α pathways. [ABSTRACT FROM AUTHOR]

This study was conducted to investigate the effect of dietary Scenedesmus ovalternus on the growth and disease resistance of gibel carp (Carassius gibelio) during overwintering. Gibel carp (initial body weight: 90.39 ± 0.33 g) were fed with diets containing 0% or 4% Scenedesmus ovalternus (DS0 and DS4) for 4 weeks during the early overwintering period, and then all fish were left unfed during the late overwintering period. A bacterial challenge test using Aeromonas hydrophila was subsequently conducted. The 4% Scenedesmus ovalternus diet had no effect on the growth of gibel carp (P > 0.05), but did improve the survival rate after the challenge (P ≤ 0.05). In the DS0 group, the bacterial challenge decreased the contents of complement 3 (C3), immunoglobulin M (IgM), interleukin 2 (IL2) and tumor necrosis factor α (TNFα) in fish (P < 0.05); in the DS4 group, the challenge increased total antioxidant capacity (T-AOC) and myeloperoxidase (MPO) activity but decreased IL2 and TNFα contents (P < 0.05). The activities of MPO and contents of C3, IgM and TNFα were higher in the DS4 group than that fed the DS0 diet after bacterial challenge (P < 0.05). Compared to pre challenge, the expression levels of toll like receptor 2 (TLR2), toll like receptor 3 (TLR3), toll like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), Toll/IL-1 receptor domain-containing adaptor protein (TIRAP), TIR-domain-containing adapter-inducing interferon β (TRIF), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor α (IκBα), transforming growth factor β (TGFβ), interleukin 1β (IL1β), tumor necrosis factor α1 (TNFα1) and interleukin 10 (IL10) in the head kidney of gibel carp were induced after challenge (P < 0.05). Gibel carp fed the DS4 diet showed lower expression of TGFβ in head kidney before the challenge and lower expression of TLR2, TLR3, TLR4, TIRAP, TRIF, IκBα, TNFα1, IL10 and TGFβ after the challenge than that fed the DS0 diet (P < 0.05). Overall, Scenedesmus ovalternus supplement enhanced the resistances of gibel carp against A. hydrophila after overwintering via the TLR signaling pathway. • The supplement of Scenedesmus ovalternus didn't have negative effect on the growth performance of gibel carp. • Scenedesmus ovalternus improved the survival rate of overwintering gibel carp after Aeromonas hydrophila infection. • Scenedesmus ovalternus improved disease resistance of overwintering gibel carp via the TLR signaling pathway. [ABSTRACT FROM AUTHOR]

Aquaculture needs effective antibiotic alternatives to control outbreaks of intestinal inflammation, as well as liver inflammation and metabolic disorder caused by enteritis. Specific metabolites have been shown to have immunomodulatory effects by the field of immunometabolism. As derivatives of the Krebs cycle metabolites, the itaconate and fumarate, 4-octyl itaconate (OI) and dimethyl fumarate (DMF) have recently attracted a lot of interest as anti-inflammatory medications. To evaluate the effects of oral administration of OI and DMF on fish growth and health, an 8-week feeding experiment followed by induction of enteritis with 2,4,6-trinitrobenzene sulfonic acid (TNBS) was carried out in gibel carp. The results showed that dietary 0.1%DMF improved the growth performance, and 0.1%OI up-regulated the abundance of beneficial intestinal microbiota. Both of OI and DMF alleviated intestinal inflammation by increasing intestinal anti-inflammatory cytokines, and relieved enteritis-induced hepatopancreas injury by inhibiting glycolysis both in vivo and in vitro. The 0.1%DMF also enhanced the tight junction and altered the microbiota to maintain the intestinal barrier. Collectively, dietary supplementation with 0.1% OI and DMF might be novel strategies to prevent enteritis and intestinal inflammation-induced hepatopancreas damage in gibel carp. [Display omitted] • Dietary 0.1%DMF improved the growth performance. • Both 0.1% OI and 0.1% DMF alleviated TNBS-induced intestinal inflammation in gibel carp. • DMF enhanced the tight junction and altered the microbiota to maintain the intestinal barrier. • OI and DMF alleviated enteritis-induced liver injury by inhibiting glycolysis both in vivo and in vitro. [ABSTRACT FROM AUTHOR]

Previous studies have shown that emodin (EMO) has a wide range of pharmacological activities, with the potential to protect against a variety of diseases. However, it is not clear whether EMO can alleviate impairment induced by acute hypoxia in gibel carp. Thus, an acute hypoxia experiment was conducted using gibel carp fed with EMO diets for eight weeks. The results showed that EMO decreased hypoxia signaling by down-regulating protein levels of hypoxia-inducible factor (HIF-1α). This also protected the liver from oxidative damage induced by acute hypoxia, as indicated by the upregulation of mRNA levels and antioxidant enzyme activity of genes related to nuclear factor erythroid 2-related factor 2 (Nrf2) signaling. Moreover, EMO also inhibited endoplasmic reticulum (ER) stress in the liver and hypothalamus induced by acute hypoxia. EMO enhanced autophagy and inhibited apoptosis in gibel carp by mediating the AMPK/mTOR signaling pathway. Overall, EMO could alleviate impairment in gibel carp induced by acute hypoxia via the AMPK/mTOR pathway. [Display omitted] • Acute hypoxia induced oxidative stress, ER stress and apoptosis in gibel carp. • EMO decreased hypoxia signaling by down-regulating protein levels of HIF-1α. • EMO improved antioxidant defense as well as inhibited ER stress effects. • Autophagy and inhibited apoptosis was enhanced by EMO in gibel carp. • EMO exerts protective effects by regulating Nrf2/Keap1 and AMPK/mTOR pathways. [ABSTRACT FROM AUTHOR]

• Endoplasmic reticulum was a major target organelle for Cd-exposed toxicity in gibel carp. • Slight time-dependent effects occurred with the extent of Cd exposure duration. • F strain showed higher stress and more efficient antioxidant defense than A strain. • Cd exposure triggered dissimilar responses on autophagy and apoptosis between strains. Previous studies illustrated that gibel carp F strain displays better lipid mobilization and antioxidant ability and compared to the A strain. We therefore hypothesized that the F strain would exhibit superior defense to cadmium exposure. Comparative studies were conducted between A and F strains using plasma stress biomarkers, histological observations, and analysis of hepatic molecular events to examine exposure to waterborne Cd (11.9 mg L−1) for 48 h and 96 h. Waterborne Cd exposure stimulated stress response and hepatic metallothionein mRNA induction in both gibel carp strains confirming exposure. Antioxidant responses were stimulated to counteract Cd toxicity, suggested by the upregulation of mRNA levels of genes associated with nuclear factor erythroid 2-related factor 2 (nrf2) signaling. Cd exposure induced endoplasmic reticulum (ER) stress, meanwhile, branches of genes in unfolded protein response (UPR) were activated. Slight time-dependent effects were implied by greater ER stress, UPR, and apoptosis signals with the duration of Cd exposure. Genotype-specific effects were identified, revealing that the F strain showed greater stress at 96 h exposure and higher antioxidant response compared to the A strain, as indicated by the mRNA levels of genes in nrf2 signaling. ER stress and UPR were also stronger in the F strain after Cd exposure. In contrast, the A strain showed higher autophagy and apoptosis response compared to the F strain. Collectively, combined autophagy and apoptosis were triggered under ER stress, which might serve as defense strategies in both gibel carp strains. The F strain showed greater antioxidant detoxification response and UPR to mitigate Cd toxicity, whereas excessive ER stress contributed to higher autophagy and apoptosis in the A strain. The present study uncovered the differential regulation and defense strategies in fish strains exposed to metal exposure. [ABSTRACT FROM AUTHOR]

Previous studies demonstrated that gibel carp A strain was more susceptible to herpesvirus infection than other strains. Thus, we hypothesized that F strain might display better defense responses than the A strain against cadmium (Cd) exposure. To test our hypothesis, gibel carp A strain and F strain were exposed to three diets comprising of different concentrations of Cd for 8 weeks to compare their resistances to Cd. Comprehensive evaluations on biochemical, physiological and histological responses were conducted post-exposure. Results showed that no adverse effects and differences were observed on growth in two strains of gibel carp, compromising of the remarkable hepatoxicity-caused liver damage as shown by histological observations. Dietary Cd exposure stimulated antioxidant defense in the liver to counteract the Cd hepatoxicity, especially in the F strain. Activation of ER stress response positively stimulated the autophagy, then triggering apoptosis in fish after dietary Cd exposure. Thus, Cd-induced autophagy served as a protective strategy to alleviate hepatoxicity, but overaction of ER stress also triggered irreparable cell death via apoptosis. Cd induced dysregulation of lipid accumulation, which might be a common mechanism in response to hepatoxicity. Last but not least, the F strain showed stronger response on antioxidant, ER stress and autophagy, but apoptosis were remitted compared with the A strain, implying the F strain showed stronger response but better defense strategies to dietary Cd exposure. Our finding provides useful information for genetic breeding in aquaculture, and ultimately contribute to the safety assessment of aquatic products for human consumption. Image 1 • Antioxidant responses may be one mechanism to counter Cd toxicity. • Apoptosis resulting from Cd exposure is implicated with ER stress and autophagy. • Chronic dietary Cd triggered lipid accumulation in gibel carp. • F strain showed better defense strategies against Cd exposure than A strain. [ABSTRACT FROM AUTHOR]