The present study evaluated the effects of increasing the dietary levels of EPA and DHA in Atlantic salmon (Salmo salar) reared in sea cages, in terms of growth performance, welfare, robustness and overall quality. Fish with an average starting weight of 275 g were fed one of four different diets containing 10, 13, 16 and 35 g/kg of EPA and DHA (designated as 1·0, 1·3, 1·6 and 3·5 % EPA and DHA) until they reached approximately 5 kg. The 3·5 % EPA and DHA diet showed a significantly beneficial effect on growth performance and fillet quality compared with all other diets, particularly the 1 % EPA and DHA diet. Fish fed the diet containing 3·5 % EPA and DHA showed 400–600 g higher final weights, improved internal organ health scores and external welfare indicators, better fillet quality in terms of higher visual colour score and lower occurrence of dark spots and higher EPA and DHA content in tissues at the end of the feeding trial. Moreover, fish fed the 3·5 % EPA and DHA diet showed lower mortality during a naturally occurring cardiomyopathy syndrome outbreak, although this did not reach statistical significance. Altogether, our findings emphasise the importance of dietary EPA and DHA to maintain good growth, robustness, welfare and fillet quality of Atlantic salmon reared in sea cages.

There is limited knowledge about the metabolism and function of n-3 very-long-chain PUFA (n-3 VLC-PUFA) with chain lengths ≥ 24. They are known to be produced endogenously in certain tissues from EPA and DHA and not considered to originate directly from dietary sources. The aim of this study was to investigate whether n-3 VLC-PUFA from dietary sources are bio-available and deposited in tissues of rat, fish and mouse. Rats were fed diets supplemented with a natural fish oil (FO) as a source of low dietary levels of n-3 VLC-PUFA, while Atlantic salmon and mice were fed higher dietary levels of n-3 VLC-PUFA from a FO concentrate. In all experiments, n-3 VLC-PUFA incorporation in organs was investigated. We found that natural FO, due to its high EPA content, to a limited extent increased endogenous production of n-3 VLC-PUFA in brain and eye of mice with neglectable amounts of n-3 VLC-PUFA originating from diet. When higher dietary levels were given in the form of concentrate, these fatty acids were bio-available and deposited in both phospholipids and TAG fractions of all tissues studied, including skin, eye, brain, testis, liver and heart, and their distribution appeared to be tissue-dependent, but not species-specific. When dietary EPA and DHA were balanced and n-3 VLC-PUFA increased, the major n-3 VLC-PUFA from the concentrate increased significantly in the organs studied, showing that these fatty acids can be provided through diet and thereby provide a tool for functional studies of these VLC-PUFA.

Excessive hepatic glycogen accumulation commonly impairs hepatocytes function and further produces negative effects on growth and health status of carnivorous fish. A 9-week feeding trial was conducted to explore the potential regulation of resveratrol (RSV) on high-carbohydrate-induced glycogen deposition and immune response of largemouth bass. Results showed that high dietary carbohydrate (10 % inclusion of starch) led to hepatic glycogen accumulation and post-prandial hyperglycemia compared with the diet with 5 % starch, which was both alleviated with the inclusion of RSV. The use of RSV promoted the expression of sirtuin 1, which was down-regulated by high dietary carbohydrate. Meanwhile, RSV inclusion promoted the expression of genes involved in insulin pathway and glycolysis and inhibited the expression of gluconeogenesis-related genes. Additionally, high dietary carbohydrate significantly reduced lysozyme content but increased complement C4 content, which were both reversed with RSV supplementation. Meanwhile, RSV inclusion inhibited the expression of pro-inflammatory cytokines but promoted anti-inflammatory cytokines expression, compared with the high carbohydrate treatment. In conclusion, RSV inclusion was beneficial in alleviating high-dietary-carbohydrate-induced glycogen accumulation and immune response in largemouth bass.

Choline plays a crucial role in hepatic lipid homeostasis by acting as a major methyl-group donor. However, despite this well-accepted fact, no study has yet explored how choline’s methyl-donor function contributes to preventing hepatic lipid dysregulation. Moreover, the potential regulatory role of Ire-1α, an ER-transmembrane transducer for the unfolded protein response (UPRer), in choline-mediated hepatic lipid homeostasis remains unexplored. Thus, this study investigated the mechanism by which choline prevents hepatic lipid dysregulation, focusing on its role as a methyl-donor and the involvement of Ire-1α in this process. To this end, a model animal for lipid metabolism, yellow catfish (Pelteobagrus fulvidraco) were fed two different diets (adequate or deficient choline diets) in vivo for 10 weeks. The key findings of studies are as follows: 1. Dietary choline, upregulated selected lipolytic and fatty acid β-oxidation transcripts promoting hepatic lipid homeostasis. 2. Dietary choline ameliorated UPRer and prevented hepatic lipid dysregulation mainly through ire-1α signalling, not perk or atf-6α signalling. 3. Choline inhibited the transcriptional expression level of ire-1α by activating site-specific DNA methylations in the promoter of ire-1α. 4. Choline-mediated ire-1α methylations reduced Ire-1α/Fas interactions, thereby further inhibiting Fas activity and reducing lipid droplet deposition. These results offer a novel insight into the direct and indirect regulation of choline on lipid metabolism genes and suggests a potential crosstalk between ire-1α signalling and choline-deficiency-induced hepatic lipid dysregulation, highlighting the critical contribution of choline as a methyl-donor in maintaining hepatic lipid homeostasis.

N-3 long-chain PUFA (LC-PUFA) and probiotics are generally considered to induce health benefits. The objective was to investigate (1) the impact of fish oil and/or probiotics on serum fatty acids (sFA), (2) the interaction of sFA with low-grade inflammation and (3) the relation of sFA to the onset of gestational diabetes mellitus (GDM). Pregnant women with overweight/obesity were allocated into intervention groups with fish oil + placebo, probiotics + placebo, fish oil + probiotics or placebo + placebo in early pregnancy (fish oil: 1·9 g DHA and 0·22 g EPA, probiotics: Lacticaseibacillus rhamnosus HN001 and Bifidobacterium animalis ssp. lactis 420, 1010 CFU, each daily). Blood samples were collected in early (n 431) and late pregnancy (n 361) for analysis of fatty acids in serum phosphatidylcholine (PC), cholesteryl esters (CE), TAG and NEFA with GC and high-sensitivity C-reactive protein and GlycA by immunoassay and NMR spectroscopy, respectively. GDM was diagnosed according to 2 h 75 g oral glucose tolerance test. EPA in PC, CE and TAG and DHA in PC, CE, TAG and NEFA were higher in fish oil and fish oil + probiotics groups compared with placebo. EPA in serum NEFA was lower in women receiving probiotics compared with women not receiving. Low-grade inflammation was inversely associated with n-3 LC-PUFA, which were related to an increased risk of GDM. Fish oil and fish oil + probiotics consumption increase serum n-3 LC-PUFA in pregnant women with overweight/obesity. Although these fatty acids were inversely related to inflammatory markers, n-3 LC-PUFA were linked with an increased risk for GDM.

A short-term 2-week (2w) and long-term 8-week (8w) feeding trial was conducted to investigate the effects of low-starch (LS) and high-starch (HS) diets on the growth performance, metabolism and liver health of largemouth bass (Micropterus salmoides). Two isonitrogenous and isolipidic diets containing two levels of starch (LS, 9·06 %; HS, 13·56 %) were fed to largemouth bass. The results indicated that HS diet had no significant effects on specific growth rate during 2w, whereas significantly lowered specific growth rate at 8w. HS diet significantly increased hepatic glycolysis and gluconeogenesis at postprandial 24 h in 2w. The hepatosomatic index, plasma alkaline phosphatase, total bile acid (TBA) levels, and hepatic glycogen, TAG, total cholesterol, TBA, and NEFA contents were significantly increased in the HS group at 2w. Moreover, HS diet up-regulated fatty acid and TAG synthesis-related genes and down-regulated TAG hydrolysis and β-oxidation-related genes. Therefore, the glucolipid metabolism disorders resulted in metabolic liver disease induced by HS diet at 2w. However, the up-regulation of bile acid synthesis, inflammation and energy metabolism-related genes in 2w indicated that largemouth bass was still in a state of ‘self-repair’ response. Interestingly, all the metabolic parameters were returned to homoeostasis, with up-regulation of intestinal glucose uptake and transport-related genes, even hepatic histopathological analysis showed no obvious abnormality in the HS group in 8w. In conclusion, HS feed induced short-term acute metabolic disorder, but long-term metabolic adaptation to HS diet was related to repairing metabolism disorders via improving inflammatory responses, bile acid synthesis and energy metabolism. These results strongly indicated that the largemouth bass owned certain adaptability to HS diet.

A high circulating cholesterol concentration is considered an important risk factor for the development of CVD. Since lean fish intake and fish protein supplementation have been associated with lower cholesterol concentration in some but not all clinical studies, the main aim of this study was to investigate the effect of diets containing proteins from fish muscles and fish by-products on the serum/plasma total cholesterol (TC) concentration in rodents. A systematic literature search was performed using the databases PubMed, Web of Science and Embase, structured around the population (rodents), intervention (type of fish and fraction, protein dose and duration), comparator (casein) and the primary outcome (circulating TC). Articles were assessed for risk of bias using the SYRCLE’s tool. A meta-analysis was conducted in Review Manager v. 5·4·1 (the Cochrane Collaboration) to determine the effectiveness of proteins from fish on the circulating TC concentration. Thirty-nine articles were included in the systematic review and meta-analysis, with data from 935 rodents. The risk of bias is unclear since few of the entries in the SYRCLE’s tool were addressed. Consumption of proteins from fish resulted in a significantly lower circulating TC concentration when compared with control groups (mean difference −0·24 mmol/l, 95 % CI − 0·34, −0·15, P < 0·00001), with high statistical heterogeneity (I2 = 71 %). To conclude, proteins from fish muscles and by-products show promise as a functional dietary ingredient or supplement by preventing high cholesterol concentration in rodents, thus reducing one of the most important risk factors for developing CVD.

The study was conducted to determine the effects of three dietary Se sources, such as sodium-selenite (S-S), seleno-yeast (S-Y) and seleno-methionine (S-M), on Se concentration, glutathione peroxidase (GPX) and TXNRD activities, and mRNA expression of fifteen representative selenoproteins, and protein expression of four endoplasmic reticulum-resided selenoproteins in a wide range of tissues of yellow catfish. Compared with S-S and S-M groups, dietary S-Y significantly decreased growth performance and feed utilisation of yellow catfish. Dietary Se sources significantly influenced Se contents in the spleen, dorsal muscle and the kidney, GPX activities in spleen, kidney, intestine, muscle and mesenteric fat, and TXNRD activities in the heart, intestine and mesenteric fat. Among ten tested tissues, dietary Se sources influenced mRNA expression of GPX4 and SELENOK in three tissues; GPX3, SELENOS and TXNRD2 in four tissues; SELENOF, SELENON and DIO2 in five tissues; SELENOM, GPX1/2 and TXNRD3 in six tissues; SELENOW in seven tissue and SELENOP and SELENOT in eight tissues. Based on these observations above, S-S and S-M seem to be suitable Se sources for improving growth performance and feed utilisation of yellow catfish. Dietary Se sources differentially influence the expression of selenoproteins in various tissues of yellow catfish. For the first time, we determined the expression of selenoproteins in fish in responses to dietary Se sources, which contributes to a better understanding of the functions and regulatory mechanisms of selenoporteins.

Nordic Nutrition Recommendations recommend reducing red and processed meat and increasing fish consumption, but the impact of this replacement on mortality is understudied. This study investigated the replacement of red and processed meat with fish in relation to mortality. Of 83 304 women in the Norwegian Women and Cancer Study (NOWAC) study, 9420 died during a median of 21·0 years of follow-up. The hazard ratios (HR) for mortality were estimated using Cox proportional hazards regression with analyses stratified on red and processed meat intake due to non-linearity. Higher processed meat (> 30 g/d), red and processed meat (> 50 g/d), and fatty fish consumption were associated with higher mortality, while red meat and lean fish consumption were neutral or beneficial. Among women with higher processed meat intake (> 30 g/d), replacing 20 g/d with lean fish was associated with lower all-cause (HR 0·92, 95 % CI 0·89, 0·96), cancer (HR 0·92, 95 % CI 0·88, 0·97) and CVD mortality (HR 0·82, 95 % CI 0·74, 0·90), while replacing with fatty fish was associated with lower CVD mortality (HR 0·87, 95 % CI 0·77, 0·97), but not with all-cause or cancer mortality. Replacing processed meat with fish among women with lower processed meat intake (≤ 30 g/d) or replacing red meat with fish was not associated with mortality. Replacing processed meat with lean or fatty fish may lower the risk of premature deaths in Norwegian women, but only in women with high intake of processed meat. These findings suggest that interventions to reduce processed meat intake should target high consumers.

Hypercholesterolaemia is a major risk factor for CVD. Fish intake is associated with lower risk of CVD, whereas supplementation with n-3 long-chain PUFA (LC-PUFA) has little effect on the cholesterol concentration. We therefore investigated if cetoleic acid (CA), a long-chain MUFA (LC-MUFA) found especially in pelagic fish species, could lower the circulating total cholesterol (TC) concentration in rodents. A systematic literature search was performed using the databases PubMed, Web of Science and Embase, structured around the population (rodents), intervention (CA-rich fish oils or concentrates), comparator (diets not containing CA) and the primary outcome (circulating TC). Articles were assessed for risk of bias using the SYRCLE’s tool. A meta-analysis was conducted in Review Manager v. 5.4.1 (the Cochrane Collaboration) to determine the effectiveness of consuming diets containing CA-rich fish oils or concentrates on the circulating TC concentration. Twelve articles were included in the systematic review and meta-analysis, with data from 288 rodents. Consumption of CA-rich fish oils and concentrates resulted in a significantly lower circulating TC concentration relative to comparator groups (mean difference −0·65 mmol/l, 95 % CI (−0·93, −0·37), P < 0·00001), with high statistical heterogeneity (I2 = 87 %). The risk of bias is unclear since few of the entries in the SYRCLE’s tool were addressed. To conclude, intake of CA-rich fish oils and concentrates prevents high cholesterol concentration in rodents and should be further investigated as functional dietary ingredients or supplements to reduce the risk for developing CVD in humans.

Milk, dairy products, and fish are the main sources of iodine in the UK. Plant-based products are increasingly popular, especially with young women, which may affect iodine intake as they are naturally low in iodine; this is concerning as iodine is required for fetal brain development. We, aimed to (i) assess the iodine fortification of products sold as alternatives to milk, yoghurt, cheese and fish through a cross-sectional survey of UK retail outlets in 2020, and (ii) model the impact of substitution with such products on iodine intake, using portion-based scenarios. We identified 300 products, including plant-based alternatives to: (i) milk (n 146); (ii) yoghurt (n 76); (iii) cheese (n 67) and (iv) fish (n 11). After excluding organic products (n 48), which cannot be fortified, only 28 % (n 29) of milk alternatives and 6 % (n 4) of yoghurt alternatives were fortified with iodine, compared with 88 % (n 92) and 73 % (n 51), respectively, with Ca. No cheese alternative was fortified with iodine, but 55 % were fortified with Ca. None of the fish alternatives were iodine fortified. Substitution of three portions of dairy product (milk/yoghurt/cheese) per day with unfortified alternatives would reduce the iodine provided by 97·9 % (124 v. 2·6 µg) and substantially reduce the contribution to the adult intake recommendation (150 µg/d; 83 v. 1·8 %). Our study highlights that the majority of plant-based alternatives are not iodine fortified and that the use of unfortified alternatives put consumers at risk of iodine deficiency.

Inulin affects nutrition and metabolism in many animals. Although inulin is widely used in the diet of teleosts, its mechanism of action is unknown. Here, we investigated the effect of inulin (2 %) on the intestinal microbiome and metabolism in rainbow trout (Oncorhynchus mykiss) selected for growth and survival when fed a 100 % plant-based diet (suave) and a control line (temoin). Metabolic responses to the two factors (line and inulin) in liver, intestine, muscle and adipose were tissue-specific, with line and interaction between the two factors influencing overall expression in liver. In the intestine, inulin and line and in muscle, line influenced the expression of metabolic genes. Microbiota between the mucus and digestive contents was significantly different, with genera from Proteobacteria being more abundant in the mucus, whereas genera from the Firmicutes and Planctomycetes being more abundant in contents. Effect of inulin and interaction between factors on the microbiome was evident in contents. The significant taxa of control and inulin-fed groups differed greatly with Streptococcus and Weissella being significantly abundant in the inulin-fed group. There was a general trend showing higher levels of all SCFA in temoin group with propionic acid levels being significantly higher. An operational taxonomic unit (OTU) belonging to the Ruminococcaceae was significantly abundant in suave. The tissue-specific correlations between OTU and gene expression may indicate the link between microbiome and metabolism. Together, these results suggest that line and inulin impact the gene expression in a tissue-specific manner, possibly driven by specific OTUs enriched in inulin-fed groups and suave.

Maternal fish consumption exposes the fetus to beneficial nutrients and potentially adverse neurotoxicants. The current study investigated associations between maternal fish consumption and child neurodevelopmental outcomes. Maternal fish consumption was assessed in the Seychelles Child Development Study Nutrition Cohort 1 (n 229) using 4-day food diaries. Neurodevelopment was evaluated at 9 and 30 months, and 5 and 9 years with test batteries assessing twenty-six endpoints and covering multiple neurodevelopmental domains. Analyses used multiple linear regression with adjustment for covariates known to influence child neurodevelopment. This cohort consumed an average of 8 fish meals/week and the total fish intake during pregnancy was 106·8 (sd 61·9) g/d. Among the twenty-six endpoints evaluated in the primary analysis there was one beneficial association. Children whose mothers consumed larger quantities of fish performed marginally better on the Kaufman Brief Intelligence Test (a test of nonverbal intelligence) at age 5 years (β 0·003, 95 % CI (0, 0·005)). A secondary analysis dividing fish consumption into tertiles found no significant associations when comparing the highest and lowest consumption groups. In this cohort, where fish consumption is substantially higher than current global recommendations, maternal fish consumption during pregnancy was not beneficially or adversely associated with children’s neurodevelopmental outcomes.

Observational evidence linking dietary n-3 PUFA intake and health outcomes is limited by a lack of robust validation of dietary intake using blood n-3 PUFA levels and potential confounding by fish oil supplement (FOS) use. We investigated the relationship between oily fish intake, FOS use and plasma n-3 PUFA levels in 121 650 UK Biobank (UKBB) participants. Ordinal logistic regression models, adjusted for clinical and lifestyle factors, were used to quantify the contribution of dietary oily fish intake and FOS use to plasma n-3 PUFA levels (measured by NMR spectroscopy). Oily fish intake and FOS use were reported by 38 % and 31 % of participants, respectively. Increasing oily fish intake was associated with a higher likelihood of FOS use (P < 0·001). Oily fish intake ≥ twice a week was the strongest predictor of high total n-3 PUFA (OR 6·7 (95 % CI 6·3, 7·1)) and DHA levels (6·6 (6·3, 7·1). FOS use was an independent predictor of high plasma n-3 PUFA levels (2·0 (2·0, 2·1)) with a similar OR to that associated with eating oily fish < once a week (1·9 (1·8, 2·0)). FOS use was associated with plasma n-3 PUFA levels that were similar to individuals in the next highest oily fish intake category. In conclusion, FOS use is more common in frequent fish consumers and modifies the relationship between oily fish intake and plasma n-3 PUFA levels in UKBB participants. If unaccounted for, FOS use may confound the relationship between dietary n-3 PUFA intake, blood levels of n-3 PUFAs and health outcomes.

The present study investigated the effect of black soldier fly (Hermetia illucens) larvae meal (BSF) on haemolymph biochemical indicators, muscle metabolites as well as the lipid and glucose metabolism of Pacific white shrimp Litopenaeus vannamei. Four diets were formulated in which the control diet contained 25 % of fishmeal (FM) and 10 % (BSF10), 20 % (BSF20), and 30 % (BSF30) of FM protein were replaced with BSF. Four hundred and eighty shrimp (0·88 ± 0·00 g) were distributed to four groups of three replicates and fed for 7 weeks. Results showed that growth performance of shrimp fed BSF30 significantly decreased compared with those fed FM, but there was no significant difference in survival among groups. The whole shrimp crude lipid content, haemolymph TAG and total cholesterol were decreased with the increasing BSF inclusion. The results of metabolomics showed that the metabolite patterns of shrimp fed different diets were altered, with significant changes in metabolites related to lipid metabolism, glucose metabolism as well as TCA cycle. The mRNA expressions of hk, pfk, pk, pepck, ampk, mcd, cpt-1 and scd1 in hepatopancreas were downregulated in shrimp fed BSF30, but mRNA expression of acc1 was upregulated. Unlike BSF30, the mRNA expressions of fas, cpt-1, fbp and 6pgd in hepatopancreas were upregulated in shrimp fed BSF20. This study indicates that BSF20 diet promoted lipid synthesis and lipolysis, while BSF30 diet weakened β-oxidation and glycolysis as well as affected the unsaturated fatty acids synthesis, which may affect the growth performance and body composition of shrimp.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters the cells after binding to the membrane-bound receptor angiotensin-converting enzyme 2 (ACE2), but this may be prevented through interception by soluble ACE2 (sACE2) or by inhibition of the ACE2 receptor, thus obstructing cell entry and replication. The main objective of this study was to investigate if fish intake affected the concentration of sACE2 in rats. The secondary aim was to evaluate the in vitro ACE2-inhibiting activity of fish proteins. Rats were fed cod muscle as 25 % of dietary protein, and blood was collected after 4 weeks of intervention. Muscle, backbone, skin, head, stomach, stomach content, intestine and swim bladder from haddock, saithe, cod and redfish were hydrolysed with trypsin before ACE2-inhibiting activity was measured in vitro. In vivo data were compared using unpaired Student’s t test, and in vitro data were compared using one-way ANOVA followed by the Tukey HSD post hoc test. The mean sACE2 concentration was 47 % higher in rats fed cod when compared with control rats (P 0·034), whereas serum concentrations of angiotensin II and TNF-α were similar between the two experimental groups. Muscle, backbone, skin and head from all four fish species inhibited ACE2 activity in vitro, whereas the remaining fractions had no effect. To conclude, our novel data demonstrate that fish intake increased the sACE2 concentration in rats and that the hydrolysed fish proteins inhibited ACE2 activity in vitro.

Se deficiency causes impaired growth of fish skeletal muscle due to the retarded hypertrophy of muscle fibres. However, the inner mechanisms remain unclear. According to our previous researches, we infer this phenomenon is associated with Se deficiency-induced high concentration of reactive oxygen species (ROS), which could suppress the target of rapamycin complex 1 (TORC1) pathway-mediated protein synthesis by inhibiting protein kinase B (Akt), an upstream protein of TORC1. To test this hypothesis, juvenile zebrafish (45 d post-fertilisation) were fed a basal Se-adequate diet or a basal Se-deficient diet or them supplemented with an antioxidant (DL-α-tocopherol acetate, designed as VE) or a TOR activator (MHY1485) for 30 d. Zebrafish fed Se-deficient diets exhibited a clear Se-deficient status in skeletal muscle, which was not influenced by dietary VE and MHY1485. Se deficiency significantly elevated ROS concentrations, inhibited Akt activity and TORC1 pathway, suppressed protein synthesis in skeletal muscle, and impaired hypertrophy of skeletal muscle fibres. However, these negative effects of Se deficiency were partly (except that on ROS concentration) alleviated by dietary MHY1485 and completely alleviated by dietary VE. These data strongly support our speculation that Se deficiency-induced high concentration of ROS exerts a clear inhibiting effect on TORC1 pathway-mediated protein synthesis by regulating Akt activity, thereby restricting the hypertrophy of skeletal muscle fibres in fish. Our findings provide a mechanistic explanation for Se deficiency-caused retardation of fish skeletal muscle growth, contributing to a better understanding of the nutritional necessity and regulatory mechanisms of Se in fish muscle physiology.