The present study investigated whether dietary n-3 very-long-chain PUFA (n-3 VLC-PUFA) could increase skin and bone mineralisation in Atlantic salmon (Salmo salar) in vivo and examined their potential effects on human osteoblast proliferation and differentiation in vitro. Atlantic salmon were fed different dietary levels of n-3 VLC-PUFA, and changes in tissue n-3 VLC-PUFA composition, skeletal morphology, skin and bone mineral content, bone mineral density (BMD) and gene expression patterns were examined. Additionally, in vitro experiments using human foetal osteoblast cells were conducted to investigate the potential influence of n-3 VLC-PUFA supplementation on cell proliferation, osteogenic differentiation and cytokine expression. The results demonstrated that increasing the dietary levels of n-3 VLC-PUFA increased the mineral content of vertebrae and BMD in salmon, with subtle yet significant impacts on the expression of genes involved in bone-related processes. Furthermore, in vitro experiments showed a potential contextual influence of n-3 VLC-PUFA supplementation on gene expression of osteogenic markers and cytokine expression. Our findings indicate for the first time that n-3 VLC-PUFA may influence processes related to bone mineralisation.

Studies on longitudinal associations between diet quality and lipid and amino acid metabolism in children and adolescents are limited. We studied associations between diet quality and serum markers of lipid and amino acid metabolism in the Physical Activity and Nutrition in Children (PANIC) study. These analyses included 403 children aged 6–9 years at baseline, 360 re-examined 2 years later at age 9–11 years and 219 eight years later at age 15–17 years. Food intake was recorded over 4 days, and diet quality was assessed using the Finnish Children Healthy Eating Index (FCHEI). Fasting serum fatty acids, amino acids, apolipoproteins and lipoprotein particle sizes were analysed via NMR spectroscopy. Linear mixed-effects models, adjusted for sex, age, body fat percentage, pubertal stage and physical activity were used to analyse the associations. Better diet quality was linked to increased serum PUFA and reduced saturated and MUFA, alanine and VLDL particle size. Consuming more vegetables, fruits, berries, vegetable oils and margarine with at least 60 % fat, fish and whole grains is associated with higher serum PUFA, lower SFA and smaller VLDL particles. Conversely, consuming higher-fat dairy products and sugary products is associated with higher saturated and MUFA, branched-chain and aromatic amino acids and larger VLDL particles. A diet rich in fruits, vegetables, unsaturated fats and fibre, with reduced sugar consumption, promotes favourable metabolic changes relevant to cardiometabolic health.

Accumulation of exogenous fatty acids such as the long-chain n-11 MUFA cetoleic acid (CA, C22:1n-11) may induce functional changes, through direct effects or by affecting the amounts of other fatty acids through changes in catabolic and anabolic processes including desaturation of fatty acids or by other processes. The primary aim of this study was to investigate if dietary CA was absorbed and accumulated in a TAG-rich tissue for storage (white adipose tissue), a stable phospholipid-rich tissue (brain), metabolically active tissues (liver and skeletal muscle) or circulating in the blood (blood cells) and metabolised. Secondary aims included investigating any effects on the levels of EPA and DHA. Eighteen male Zucker diabetic Sprague Dawley (ZDSD) rats were fed diets with herring oil (HERO) containing 0·70 % CA or anchovy oil (ANCO) devoid of CA, or a control diet with soyabean oil for 5 weeks. The HERO and ANCO diets contained 0·35 and 0·37 wt% EPA + DHA, respectively. Data were analysed using one-way ANOVA. CA from dietary HERO was absorbed, and CA and two chain-shortened metabolites were found in blood cells, liver, white adipose tissue (WAT) and muscle, but n-11 MUFAs were not found in the brain. The concentrations of EPA and DHA were similar in liver lipids (TAG, cholesteryl esters and NEFA) as well as in WAT, muscle and brain from rats fed the HERO or ANCO diets. To conclude, CA was taken up by tissues but did not affect levels of EPA and DHA in this diabetic rat model.

This interventional single-centre prospective open-label study aims to evaluate the effects of a vegan diet, compared with a vegetarian and omnivorous diet, on metabolic parameters, insulin sensitivity, and liver and kidney steatosis in healthy adults. The study included fifty-three omnivorous participants aged 18–40 years, BMI 18–30 kg/m2, without any chronic disease, chronic medication use, active smoking or significant alcohol consumption. All participants were omnivorous at baseline and selected to continue an omnivorous diet or transition to a vegetarian or vegan diet, with follow-up over 6 months. Anthropometric measurements, biochemical parameters and liver and kidney steatosis were assessed at baseline and after six months using MRI-proton density fat fraction. Primary outcomes included changes in liver and kidney steatosis, while secondary outcomes were alterations in anthropometric and biochemical markers. Among fifty-three participants, eighteen followed an omnivorous diet, twenty-one adopted a vegetarian diet and fourteen transitioned to a vegan diet. Dietary interventions did not result in statistically significant changes in BMI, fat mass, fat percentage or muscle mass over 6 months. However, statistically significant improvements in systolic and diastolic blood pressure, favouring the vegan diet, were observed. We aimed to control for potentially confounding variables to ensure the reliability of these findings. We have demonstrated a better decline in steatosis at the lower kidney pole, the total hilus and the Liver 6 index in vegans. We demonstrated that a plant-based diet is associated with improvements in several metabolic parameters and may reduce liver and kidney steatosis.

With the widespread use of high-fat diets (HFD) in aquaculture, the adverse effects of HFD on farmed fish are becoming increasingly apparent. Creatine has shown potential as a green feed additive in farmed fish; however, the potential of dietary creatine to attenuate adverse effects caused by high-fat diets remains poorly understood. To address such gaps, this study was conducted to investigate the mitigating effect of dietary creatine on HFD-induced disturbance on growth performance, hepatic lipid metabolism, intestinal health and muscle quality of juvenile largemouth bass. Three diets were formulated: a control diet (10·20 % lipid), a high-fat diet (HFD, 18·31 % lipid) and HFD with 2 % creatine (HFD + creatine). Juvenile largemouth bass (3·73 (sem 0·01) g) were randomly assigned to three diets for 10 weeks. The key findings were as follows: (1) the expression of muscle growth-related genes and proteins was stimulated by dietary creatine, which contributes to ameliorate the adverse effects of HFD on growth performance; (2) dietary creatine alleviates HFD-induced adverse effects on intestinal health by improving intestinal health, which also enhances feed utilisation efficiency; (3) dietary creatine causes excessive lipid deposition, mainly via lipolysis and β-oxidation. Notably, this study also reveals a previously undisclosed effect of creatine supplementation on improving muscle quality. Together, for the first time from a comprehensive multiorgan or tissue perspective, our study provides a feasible approach for developing appropriate nutritional strategies to alleviate the adverse effects of HFD on farmed fish, based on creatine supplementation.

Evidence indicates hypervitaminosis A may be attributed to overconsumption of natural preformed vitamin A (VA) and overlapping VA intervention strategies. Hypervitaminosis A can disrupt metabolic processes; however, the extent and mechanisms of these impacts are not well understood. This study aims to assess metabolic differences related to hypervitaminosis A and VA supplementation by performing metabolomics analysis. A subsample of South African preschoolers participating in the country’s VA supplementation programme was selected. Participants were divided into two groups: adequate VA (n 15; 0·59–0·99 µmol/g total liver reserve and high VA (n 15; ≥ 1·0 µmol/g total liver reserve). Serum samples were collected at baseline and 28 d after consuming a 200 000 IU VA supplement. Lipidomics and oxylipins assays were conducted using ultraperformance LC-MS. At baseline, unsaturated lysophosphatidylcholines and unsaturated phosphatidylcholines were significantly lower in the high VA group (P < 0·05). A group-by-time interaction with VA supplementation was observed for polyunsaturated lysophosphatidylcholines and polyunsaturated phosphatidylcholines (P < 0·05). Additionally, a group effect was noted for oxylipins, and a time effect in response to VA supplementation was seen with decreased arachidonic acid and lipoxygenase- and non-enzymatically derived oxylipins (P < 0·05). Hypervitaminosis A is associated with modifications in lipids involved in cell structure and signalling, particularly unsaturated lysophosphatidylcholines and phosphatidylcholines. Further research is needed to identify the mechanisms behind these modifications, their physiological effects and their potential as biomarkers of elevated vitamin A status.

The impact of synchronising the collection and supply of breast milk produced during the day and night on improving long-term health outcomes for preterm infants is discussed, focusing on breast milk as a valuable source of melatonin, an essential synchroniser of biological rhythms.

We have used multiple regression analyses to develop a series of metabolisable energy prediction equations from chemical analyses of pig diets that can be extended to murine diets. We compiled four datasets from an extensive range of published metabolism studies with grower/finisher and adult pigs. The analytes in the datasets were increasingly complex, comprising (1) the proximate or Weende analysis, (2) the previous analysis but with neutral detergent fibre replacing crude fibre, (3) the neutral detergent fibre package plus starch and (4) the neutral detergent fibre package plus starch and sugars. Diet manufacturers routinely provide most of the analytes for batches of murine diet, or they are easily obtainable. The study uniquely compares the four analytical packages side by side. The number of records in the datasets varies from 367 to 827. With increasing analytical complexity, adjusted R2 values for metabolisable energy prediction improved from 0·751 to 0·869 and the mean absolute error from 0·422 to 0·289 kJ/g. Overall, the models’ prediction interval improved from 1 to 0·7 kJ/g, which is ± 7 to 5 % for a typical dietary metabolisable energy density of 14·8 kJ/g. Although prediction accuracy increases as one extends the range and complexity of the analytes measured, the improvement is slight and may not justify the substantial increase in analytical cost. The equations were validated for use on future datasets by k-fold analysis. Although the equations are developed from pig data, they are suitable for rat and mouse diets, based on comparable digestibility measurements, and substantially improve existing methods.

This study evaluated the effects of chenodeoxycholic acid (CDCA), a farnesoid X receptor (FXR) potential activator, on growth performance, antioxidant capacity, glucose metabolism and inflammation in largemouth bass (Micropterus salmoides) (initial body weight: 5·45 ± 0·02 g) fed a high-carbohydrate diet. Experimental diets included a positive control (5 % α-starch), a negative control (10 % α-starch) and two diets containing 10 % α-starch supplemented with either 0·05 % or 0·10 % CDCA. After 8 weeks, the high-carbohydrate diet reduced growth performance and increased hepatosomatic and viscerosomatic indexes, which were mitigated by 0·10 % CDCA supplementation. The high-carbohydrate diet also increased hepatic glycogen and crude lipid content, both of which were reduced by 0·10 % CDCA. Furthermore, the high-carbohydrate diet-induced oxidative stress, histopathological changes and reduced liver lysozyme activity, which were ameliorated by CDCA supplementation. Molecular analysis showed that the high-carbohydrate diet suppressed FXR and phosphorylated AKT1 (p-AKT1) protein expression in the liver, downregulated insulin signalling (ira, irs, pi3kr1 and akt1), gluconeogenesis (pepck and g6pc) and glycolysis genes (gk, pk and pfkl). CDCA supplementation upregulated fxr expression, activated shp, enhanced the expression of insulin signalling and glycolytic genes (gk, pk and pfkl) and inhibited gluconeogenesis. Additionally, CDCA reduced inflammatory markers (nf-κb and il-1β) and restored anti-inflammatory mediators (il-10, iκb and tgf-β). In conclusion, 0·10 % CDCA improved carbohydrate metabolism and alleviated liver inflammation in largemouth bass fed a high dietary carbohydrate, partially through FXR activation.

Several studies have indicated a potential inverse association between caffeine intake from dietary sources – assessed through dietary questionnaires – and uric acid (UA) levels. However, to date, no study has examined the relationship between urinary caffeine metabolites, which serve as a reliable biomarker of caffeine intake and UA levels. Our aim was to evaluate the association between caffeine metabolites in urine and serum UA levels. A cross-sectional study was conducted using data from the National Health and Nutrition Examination Survey (NHANES) 2011–2012, involving 1252 individuals aged 20–80 years. The study assessed caffeine and fourteen metabolites in spot urine samples, as well as serum UA levels. Hyperuricaemia was defined as UA levels exceeding 7·0 mg/dl for men and 6·0 mg/dl for women. In logistic regression analyses, theobromine (OR: 0·99, 95 % CI: 0·980, 0·999), 3-methyluric acid (OR: 0·91, 95 % CI: 0·837, 0·996), 7-methyluric acid (OR: 0·99, 95 % CI: 0·989, 0·998) and 3-methylxanthine (OR: 0·99, 95 % CI: 0·992, 0·999) were associated with decreased odds of hyperuricaemia. In linear regression analyses, paraxanthine (β = −0·004, P = 0·006), theobromine (β = −0·004, P =< 0·001), 7-methyluric acid (β = −0·003, P = 0·003), 3,7-dimethyluric acid (β = −0·029, P = 0·024), 3-methylxanthine (β = −0·001, P = 0·038) and 7-methylxanthine (β = −0·001, P = 0·001) were inversely associated with serum UA levels. In conclusion, our results indicate that several urinary caffeine metabolites are inversely associated with UA levels. These findings should be interpreted with caution due to the small magnitude of the observed associations.

A hospital-based cross-sectional study involving children aged 2–15 years attending the obesity clinic of a tertiary care hospital from January 2016 to March 2018 was carried out to study carotid intima media thickness (cIMT) and its association with cardiometabolic risk factors in children with overweight and obesity. Secondary objective was to compare children with elevated (EcIMT) and normal cIMT (NcIMT). Out of 223 patients enrolled for the study, 102 (45·7 %) had EcIMT. Mean cIMT of the study participants was 0·41 (sd 0·13) mm. Median alanine transaminase levels (27 v. 24, P= 0·006) and proportion of patients with fatty liver (63·7 % v. 48·8 %, P= 0·025) and ≥ 3 risk factors (80·4 % v. 66·1 %, P= 0·003) were higher in the EcIMT group compared with NcIMT group. Proportion of patients with hypercholesterolemia (36·4 % v. 16 %, P= 0·024), elevated LDL-cholesterol (38·6 % v. 16 %, P= 0·013), low HDL-cholesterol (40·9 % v. 20 %, P= 0·027) and dyslipidemia (84·1 % v. 58 %, P= 0·006) was higher in the pubertal EcIMT group and those with fatty liver (63·8 % v. 45·1 %, P= 0·034) was higher in the prepubertal EcIMT group compared with pubertal and prepubertal NcIMT groups, respectively. No significant correlations were observed between cIMT and various cardiometabolic parameters. Our finding of EcIMT in nearly half of the study participants including young children is very concerning as these children are at increased risk of atherosclerotic CVD in adulthood. Interventions starting at a young age are important when trajectories are likely to be more malleable and adverse cardiometabolic phenotypes and subclinical atherosclerosis are reversible.

The World Cancer Research Fund and the American Institute for Cancer Research recommend a plant-based diet to cancer survivors, which may reduce chronic inflammation and excess adiposity associated with worse survival. We investigated associations of plant-based dietary patterns with inflammation biomarkers and body composition in the Pathways Study, in which 3659 women with breast cancer provided validated food frequency questionnaires approximately 2 months after diagnosis. We derived three plant-based diet indices: overall plant-based diet index (PDI), healthful plant-based diet index (hPDI) and unhealthful plant-based diet index (uPDI). We assayed circulating inflammation biomarkers related to systemic inflammation (high-sensitivity C-reactive protein [hsCRP]), pro-inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and anti-inflammatory cytokines (IL-4, IL-10, IL-13). We estimated areas (cm2) of muscle and visceral and subcutaneous adipose tissue (VAT and SAT) from computed tomography scans. Using multivariable linear regression, we calculated the differences in inflammation biomarkers and body composition for each index. Per 10-point increase for each index: hsCRP was significantly lower by 6·9 % (95 % CI 1·6%, 11·8%) for PDI and 9·0 % (95 % CI 4·9%, 12·8%) for hPDI but significantly higher by 5·4 % (95 % CI 0·5%, 10·5%) for uPDI, and VAT was significantly lower by 7·8 cm2 (95 % CI 2·0 cm2, 13·6 cm2) for PDI and 8·6 cm2 (95 % CI 4·1 cm2, 13·2 cm2) for hPDI but significantly higher by 6·2 cm2 (95 % CI 1·3 cm2, 11·1 cm2) for uPDI. No significant associations were observed for other inflammation biomarkers, muscle, or SAT. A plant-based diet, especially a healthful plant-based diet, may be associated with reduced inflammation and visceral adiposity among breast cancer survivors.

Modern Western diets, characterised by a substantial proportion of kilocalories derived from ultra-processed foods (UPF), have been associated with systemic inflammation. This study examines the association between UPF consumption and inflammation, assessed through alterations in C-reactive protein (CRP) concentrations, among Brazilian adolescents. This is a cross-sectional study involving a sub-sample of 6316 adolescents aged 12–17 years, participants in the Study of Cardiovascular Risk in Adolescents (ERICA), from seven capitals in Brazil. Dietary intake was assessed using a 24-hour recall, and foods were categorised based on their degree of processing according to the NOVA classification. UPF consumption was then divided into quartiles. For CRP evaluation, blood samples were collected after a 12-hour fasting period and categorised as > 3 mg/l, indicating low-grade inflammation. Poisson regression models with robust variance were employed to assess the association between UPF consumption and high CRP concentrations. High UPF consumption (highest quartile, ≥ 44·9 % kcal/d) was slightly associated with a higher prevalence of CRP after adjusting for potential confounders (prevalence ratio = 1·039; 95 % CI: 1·006, 1·073), compared with those in the lowest quartile of UPF consumption. However, when evaluating different groups of UPF separately (such as sugary beverages, processed meats and sweets), the previous association was no longer observed. These findings suggest a modest association between overall UPF consumption and early indicators of unhealthy low-grade inflammation in adolescents. Further experimental and cohort studies are necessary to clarify the role of UPF in inflammatory processes.

Studies have demonstrated that the quality and transparency of reporting clinical practice guidelines (CPG) in health care are low. This meta-research aimed to evaluate the adherence of nutrition CPG for critically ill adults to the Reporting Items for practice Guidelines in HealTh care (RIGHT) checklist and its association with the methodological quality assessed by the Appraisal of Guidelines for Research and Evaluation II (AGREE II), along with other potential publication-related factors. A systematic search for CPG until December 2024 was conducted. RIGHT and AGREE II were applied. Eleven CPG were identified, none demonstrated adherence greater than 60 % to the RIGHT checklist and the mean RIGHT score was 33·5 ± 15·5 %. There was a strong correlation between the RIGHT score and AGREE II (r 0·886). A development CPG team including methodologist and/or statistician was associated with a higher RIGHT score (48·9 ± 4·5 v. 27·2 ± 11·0), and it was higher in CPG recommended or recommended with modifications by AGREE II in comparison to those not recommended (50·1 ± 4·6 v. 37·7 ± 8·1 v. 17·0 ± 6·8), and in those with acceptable and moderate compared with those with low methodological quality (50·1 ± 4·6 v. 32·2 ± 14·5 v. 19·3 ± 6·2). It was also related to the language of publication, being higher in those published in English. The reporting completeness in CPG for critically ill adults was low, with a strong correlation with the methodological quality. High values of reporting completeness scores were observed between CPG recommended by AGREE II (with moderate or acceptable quality) and in those including a methodologist/statistician in the development team.

In this study, nine isonitrogenous experimental diets containing graded levels of carbohydrates (40 g/kg, 80 g/kg and 120 g/kg) and crude lipids (80 g/kg, 120 g/kg and 160 g/kg) were formulated in a two-factor (3 × 3) orthogonal design. A total of 945 mandarin fish with similar body weights were randomly assigned to twenty-seven tanks, and the experiment diets were fed to triplicate tanks twice daily for 10 weeks. Results showed that different dietary treatments did not significantly affect the survival rate and growth performance of mandarin fish. However, high dietary lipid and carbohydrate levels significantly decreased the protein content of the whole body and muscle of cultured fish. The lipid content of the whole body, liver and muscle all significantly increased with increasing levels of dietary lipid, while only liver lipid level was significantly affected by dietary carbohydrate level. Hepatic glycogen content increased significantly with increasing dietary carbohydrate levels. As to liver antioxidant capacity, malondialdehyde content increased significantly with increasing dietary lipid or carbohydrate content, and catalase activity showed an opposite trend. Superoxide dismutase activity increased significantly with increasing levels of dietary lipid but decreased first and then increased with increasing dietary carbohydrate levels. Additionally, the increase in both dietary lipid and carbohydrate levels resulted in a significant reduction in muscle hardness. Muscle chewiness, gumminess and shear force were only affected by dietary lipid levels and decreased significantly with increasing dietary lipid levels. In conclusion, considering all the results, the appropriate dietary lipids and carbohydrate levels for mandarin fish were 120 g/kg and 80 g/kg, respectively.

Research on the association between the Chinese visceral adiposity index (CVAI) and hyperuricaemia (HUA) is scarce, and whether the association differs by sex is unclear. This research aimed to explore sex-specific associations between CVAI and HUA and to compare CVAI’s predictive performance with other adiposity indices using data from 22 171 adults (30–79 years) in the China Multi-Ethnic Cohort study (Chongqing region). The prevalence of HUA was 20·9 % in men and 9·7 % in women. Multivariable logistic regression analyses were utilised to assess the adjusted OR and 95 % CI. After multivariable adjustment, CVAI was associated with HUA in men (OR Q4 v. Q1 = 3·31, 95 % CI 2·73, 4·03) and women (OR Q4 v. Q1 = 7·20, 95 % CI 5·12, 10·12). Moreover, significant interactions were observed between BMI and CVAI on HUA in both sexes (all Pinteraction < 0·001), with the strongest associations in those with BMI < 24·0 kg/m2. The OR (95 % CI) across different BMI groups (< 24·0, 24·0–27·9, ≥ 28·0 kg/m²) were 1·87 (1·63, 2·13), 1·65 (1·48, 1·85) and 1·30 (1·14, 1·49) for men and 2·76 (2·18, 3·51), 2·46 (1·98, 3·07) and 1·87 (1·47, 2·39) for women, respectively. Additionally, CVAI showed satisfactory predictive performance for HUA in women, with the largest area under the receiver operating characteristic curve of 0·735, but not in men (0·660). These findings suggest a close association between CVAI and HUA, particularly pronounced in those with BMI < 24·0 kg/m², and a stronger association in women than in men.

This study was designed to explore the mediating role of serum 25-hydroxyvitamin D (25(OH) D) in Triglyceride–glucose (TyG) index and hypertension (HTN). Study participants were selected from the 2001 to 2018 National Health and Nutrition Examination Survey. Firstly, we estimated the association between TyG index and serum 25(OH)D with HTN using a weighted multivariable logistic regression model and restricted cubic spline. Secondly, we used a generalised additive model to investigate the correlation between TyG index and serum 25(OH)D. Lastly, serum 25(OH)D was investigated as a mediator in the association between TyG index and HTN. There were 14 099 subjects in total. TyG index was positively and linearly associated with HTN risk, while serum 25(OH)D had a U-shaped relationship with the prevalence of HTN. When the serum 25(OH)D levels were lower than 57·464 mmol/l, the prevalence of HTN decreased with the increase of serum 25(OH)D levels. When serum 25(OH)D levels rise above 57·464 mmol/l, the risk of HTN increases rapidly. Based on the U-shaped curve, serum 25(OH)D concentrations were divided into two groups: < 57·464 and ≥57·464 mmol/l. According to the mediation analysis, when serum 25(OH)D levels reached < 57·464 mmol/l, the positive association between the TyG index and incident HTN was increased by 25(OH)D. When serum 25(OH)D levels reached ≥ 57·464 mmol/l, the negative association between the TyG index and incident HTN was increased by 25(OH)D. There was a mediation effect between the TyG index and HTN, which was mediated by 25(OH)D. Therefore, we found that the association between serum 25(OH)D levels and TyG index may influence the prevalence of HTN.