Dietary fibre is believed to provide important health benefits including protection from colorectal cancer. However, the evidence on the relationships with different dietary fibre sources is mixed and little is known about which fibre source provides the greatest benefits. We conducted a dose–response meta-analysis of prospective cohorts to summarise the relationships of different fibre sources with colorectal cancer and adenoma risks. Analyses were restricted to publications that reported all fibre sources (cereals, vegetables, fruits, legumes) to increase comparability between results. PubMed and Embase were searched through August 2018 to identify relevant studies. The summary relative risks (RR) and 95 % CI were estimated using a random-effects model. This analysis included a total of ten prospective studies. The summary RR of colorectal cancer associated with each 10 g/d increase in fibre intake were 0·91 (95 % CI 0·82, 1·00; I2 = 0 %) for cereal fibre, 0·95 (95 % CI 0·87, 1·03, I2 = 0 %) for vegetable fibre, 0·91 (95 % CI 0·78, 1·06, I2 = 43 %) for fruit fibre and 0·84 (95 % CI 0·63, 1·13, I2 = 45 %) for legume fibre. For cereal fibre, the association with colorectal cancer risk remained statistically significant after adjustment for folate intake (RR 0·89, 95 % CI 0·80, 0·99, I2 = 2 %). For vegetable and fruit fibres, the dose–response curve suggested evidence of non-linearity. All fibre sources were inversely associated with incident adenoma (per 10 g/d increase: RR 0·81 (95 % CI 0·54, 1·21) cereals, 0·84 (95 % CI 0·71, 0·98) for vegetables, 0·78 (95 % CI 0·65, 0·93) for fruits) but not associated with recurrent adenoma. Our data suggest that, although all fibre sources may provide some benefits, the evidence for colorectal cancer prevention is strongest for fibre from cereals/grains.

The objective of the present study was to investigate the effect of curcumin on insulin resistance (IR) and hepatic lipid accumulation in intra-uterine growth restriction (IUGR). Rats with a normal birth weight (NBW) or IUGR were fed basic diets (NBW and IUGR groups) or basic diets supplemented with curcumin (NBW-C and IUGR-C groups) from 6 to 12 weeks. Rats in the IUGR group showed higher levels of glucose and homeostasis model assessment for insulin resistance index (HOMA-IR) (P < 0·05) than in the NBW group. The livers of IUGR rats exhibited higher (P < 0·05) concentration of TAG and lower (P < 0·05) activities of lipolysis enzymes compared with the normal rats. In response to dietary curcumin supplementation, concentrations of serum insulin, glucose and HOMA-IR, pyruvate, TAG, total cholesterol and NEFA in the liver were decreased (P < 0·05). The concentrations of glycogen and activities of lipolysis enzymes in the liver were increased (P < 0·05) in the IUGR-C group compared with the IUGR group. These results were associated with lower (P < 0·05) phosphorylated insulin receptor substrate 1, protein kinase B or Akt, glycogen synthase kinase 3β and expressions of sterol regulatory element binding protein 1 and fatty acid synthase (FASN); decreased expressions for Cd36, sterol regulatory element binding protein 1c (Srebf1) and Fasn; increased (P < 0·05) expression of PPARα; and expressions for Ppara and hormone-sensitive lipase in the liver of IUGR-C rats than the IUGR rats. Maternal malnutrition caused IR and lipid accumulation in the liver. Curcumin supplementation prevented IR by regulating insulin signalling pathways and attenuated hepatic lipid accumulation.

l-Carnitine is essential for mitochondrial β-oxidation and has been used as a lipid-lowering feed additive in humans and farmed animals. d-Carnitine is an optical isomer of l-carnitine and dl-carnitine has been widely used in animal feeds. However, the functional differences between l- and d-carnitine are difficult to study because of the endogenous l-carnitine background. In the present study, we developed a low-carnitine Nile tilapia model by treating fish with a carnitine synthesis inhibitor, and used this model to investigate the functional differences between l- and d-carnitine in nutrient metabolism in fish. l- or d-carnitine (0·4 g/kg diet) was fed to the low-carnitine tilapia for 6 weeks. l-Carnitine feeding increased the acyl-carnitine concentration from 3522 to 10 822 ng/g and alleviated the lipid deposition from 15·89 to 11·97 % in the liver of low-carnitine tilapia. However, as compared with l-carnitine group, d-carnitine feeding reduced the acyl-carnitine concentration from 10 822 to 5482 ng/g, and increased lipid deposition from 11·97 to 20·21 % and the mRNA expression of the genes involved in β-oxidation and detoxification in the liver. d-Carnitine feeding also induced hepatic inflammation, oxidative stress and apoptosis. A metabolomic investigation further showed that d-carnitine feeding increased glycolysis, protein metabolism and activity of the tricarboxylic acid cycle and oxidative phosphorylation. Thus, l-carnitine can be physiologically utilised in fish, whereas d-carnitine is metabolised as a xenobiotic and induces lipotoxicity. d-Carnitine-fed fish demonstrates increases in peroxisomal β-oxidation, glycolysis and amino acid degradation to maintain energy homeostasis. Therefore, d-carnitine is not recommended for use in farmed animals.

The aim of this work was to study the bioavailability of fatty acids (FA), focusing on n-3 long-chain (LC) PUFA, carried by different molecular lipid species, that is, phospholipids (PL) or TAG, with three formulations based on fish oils or marine PL, providing a similar n-3 LC PUFA amount. The digestive lipolysis was first assessed using an in vitro enzymatic model. Then, intestinal absorption and enterocyte metabolism were investigated in vivo, on male Wistar rats through lymph lipid analysis. The in vitro results showed that the release of n-3 LC PUFA from lipolysis was increased by 48 % when FA were provided as PL rather than TAG. The in vivo results demonstrated that EPA and DHA from both TAG and PL were similarly absorbed and incorporated into lymph lipids. However, DHA was mainly distributed at the sn-1/3 positions of lymph TAG when provided as marine PL, whereas it was equally distributed at the three positions with marine TAG. On the whole, even if the molecular lipid species of n-3 LC PUFA did not greatly modify the in vivo digestion and absorption steps, it modulated the rearrangement of DHA on the glyceride positions of the lymph TAG, which may further impact the DHA metabolic fate and tissue accretion. Consequently, the present study has provided data which may be used to formulate lipid diets rich in DHA in the context of an insufficient consumption of n-3 PUFA in Western countries.

The fenofibrate functions in mammals could be affected by many factors such as dietary nutrient levels and physiological status. However, this phenomenon has not been well studied in fish. The goal of our study was to investigate the effect of dietary protein contents on metabolic regulation of fenofibrate in Nile tilapia. An 8-week experiment was conducted to feed fish with four diets at two protein levels (28 and 38 %) with or without the supplementation of fenofibrate (200 mg/kg body weight per d). After the trial, the body morphometric parameters, plasma biochemical parameters and quantitative PCR data were examined. These results showed that fenofibrate significantly reduced the feeding intake and weight gain rate, increased the oxidative stress (increased plasma methane dicarboxylic aldehyde) and liver : body ratio (increased hepatosomatic index) in the low protein (LP)-fed fish. In contrast, fenofibrate exhibited a lipid-lowering (reduced hepatic lipid) effect and up-regulated the expressions of the genes related to lipid catabolism, transport and anabolic metabolism in the high protein (HP)-fed fish. The present study suggested that lipid-lowering effect of fenofibrate would be strengthened in the fish fed with the HP diet containing high energy, but in the fish fed with the LP diet containing low energy, the fenofibrate treatment would cause adverse effects for metabolism. Taking together, our study showed that the metabolic regulation of fenofibrate in Nile tilapia was dependent not only on feed energy content but also on dietary nutrient composition, such as dietary protein and/or lipid levels.

The present study investigated the effects of glutamine (GLN) pretreatment on CD4+ T cell polarisation and remote kidney injury in mice with gut-derived polymicrobial sepsis. Mice were randomly assigned to three groups: normal control fed with American Institute of Nutrition (AIN)-93G diet and two sepsis groups provided with either AIN-93G-based diet or identical components, except part of casein was replaced by GLN. Mice were given their respective diets for 2 weeks. Then, mice in the sepsis groups were performed with caecal ligation and puncture and were killed 72 h after the surgery. Blood, spleens and kidneys were collected for further examination. The results showed that sepsis resulted in decreased circulating and splenic total T lymphocyte and CD4+ T cell percentages, whereas IL-4-, and forkhead box p3 (Foxp3)-expressing CD4+ T cells percentages were up-regulated. Compared with the sepsis control group, pretreatment with GLN maintained blood T and CD4+ T cells and reduced percentages of IL-4- and Foxp3-expressing CD4+ T cells. Also, a more pronounced activation and increased anti-apoptotic Bcl-2 gene expression of splenic CD4+ T cells were observed. Concomitant with the decreased plasma IL-6, keratinocyte-derived chemokine (KC) levels, the gene expression of KC, macrophage inflammatory protein-2 and renal injury biomarker kidney injury molecule-1 (Kim-1) were down-regulated when GLN was administered. These findings suggest that antecedent of GLN administration elicit a more balanced blood T helper cell polarisation, sustained T cell populations, prevented splenic CD4+ T cell apoptosis and attenuated kidney injury at late phase of polymicrobial sepsis. GLN may have benefits in subjects at risk of abdominal infection.

Intestinal barrier inflammatory damage is commonly accompanied by hypoxia. The hypothesis that dietary Acanthopanax senticosus polysaccharides (ASPS) might modulate the hypoxia-inducible factor-1α (HIF-1α) signalling pathway and contribute to attenuate intestinal injury was tested in lipopolysaccharide (LPS)-challenged piglets. Thirty-six weaned pigs were randomly allocated to one of the following three groups: (1) basal diet + saline challenge; (2) basal diet + LPS challenge; (3) basal diet with 800 mg/kg ASPS + LPS challenge. LPS was injected at 15, 18 and 21 d, and intestinal sections were sampled following blood collection at 21 d . The results showed ASPS reversed (P < 0·05) LPS-induced decrease in average daily feed intake and rise (P < 0·05) of diarrhoea incidence and index. Biochemical index reflecting gut barrier damage and function involving ileal pro-inflammatory cytokines (TNF-α and IL-1β) and enzyme activity (diamine oxidase and lactase), as well as circulatory d-xylose, was normalised (P < 0·05) in LPS-challenged piglets receiving ASPS. ASPS also ameliorated intestinal morphological deterioration of LPS-challenged piglets, proved by elevated ileal villus height (P < 0·05) and improved appearance of epithelial villus and tight junction ultrastructure. Moreover, ASPS prevented LPS-induced amplification of inflammatory mediators, achieved by depressed ileal mRNA abundance of TNF-α, inducible NO synthase and IL-1β concentration. Importantly, ileal protein expressions of HIF-1α, cyclo-oxygenase-2 (COX-2) and NFκB p65 were also suppressed with ASPS administration (P < 0·05). Collectively, these results suggest the improvement of mucosal inflammatory damage and diarrhoea in immune stress piglets is possibly associated with a novel finding where HIF-1α/COX-2 pathway down-regulation is involved in NFκB p65-inducible releasing of inflammatory cytokines by dietary ASPS.

Coccidial infections reduce fat-soluble vitamin status and bone mineralisation in broiler chickens. We hypothesised that broilers infected with Eimeria maxima would benefit from increased dietary supplementation with vitamin D (vitD) or with 25-hydroxycholecalciferol (25(OH)D3 or 25D3). Broilers were assigned to diets with low (L) or commercial (M) vitD levels (25 v. 100 μg/kg) supplemented as cholecalciferol (D3) or 25D3. At day 11 of age, birds were inoculated with water or 7000 E. maxima oocysts. Pen performance was calculated over the early (days 1–6), acute (days 7–10) and recovery periods (days 11–14) post-infection (pi). At the end of each period, six birds per treatment were dissected to assess long bone mineralisation, plasma levels of 25D3, Ca and P, and intestinal histomorphometry. Parasite replication and transcription of cytokines IL-10 and interferon-γ (IFN-γ) were assessed at day 6 pi using quantitative PCR. Performance, bone mineralisation and plasma 25D3 levels were significantly reduced during infection (P < 0·05). M diets or diets with 25D3 raised plasma 25D3, improved performance and mineralisation (P < 0·05). Offering L diets compromised feed efficiency pi, reduced femur breaking strength and plasma P levels at day 10 pi in infected birds (P < 0·05). Contrastingly, offering M diets or diets with 25D3 resulted in higher parasite loads (P < 0·001) and reduced jejunal villi length at day 10 pi (P < 0·01), with no effect on IL-10 or IFN-γ transcription. Diets with M levels or 25D3 improved performance and mineralisation, irrespective of infection, while M levels further improved feed efficiency and mineralisation in the presence of coccidiosis.

Vascular surgery patients are nutritionally vulnerable. Various malnutrition screening and assessment tools are available; however, none has been developed or validated in vascular patients. The present study aimed to: (1) investigate the validity of four commonly administered malnutrition screening tools (Malnutrition Screening Tool (MST), Malnutrition Universal Screening Tool (MUST), Nutrition Risk Screen-2002 (NRS-2002) and the Mini-Nutritional Assessment – Short Form (MNA-SF) and an assessment tool (the Patient-Generated Subjective Global Assessment (PG-SGA)) compared against a comprehensive dietitian’s assessment and (2) evaluate the ability of the instruments to predict outcomes. Vascular inpatients were screened using the four malnutrition screening tools and assessed using the PG-SGA. Each was assessed by a dietitian incorporating nutritional biochemistry, anthropometry and changes in dietary intake. Diagnostic accuracy, consistency and predictive ability were determined. A total of 322 (69·3 % male) patients participated, with 75 % having at least one parameter indicating nutritional deficits. No instrument achieved the a priori levels for sensitivity (14·9–52·5 %). Neither tool predicted EuroQoL 5-dimension 5-level score. All tools except the MNA-SF were associated with length of stay (LOS); however, the direction varied with increased risk of malnutrition on the MUST and NRS-2002 being associated with shorter LOS (P=0·029 and 0·045) and the reverse with the MST and PG-SGA (P=0·005 and <0·001). The NRS-2002 was associated with increased risk of complications (P=0·039). The MST, NRS-2002 and PG-SGA were predictive of discharge to an institution (P=0·004, 0·005 and 0·003). The tools studied were unable to identify the high prevalence of undernutrition; hence, vascular disease-specific screening and/or assessment tools are warranted.

As only limited evidence is available for potential benefits of n-3 PUFA supplementation in patients with peripheral arterial disease (PAD), we studied the effects of 4 g n-3 PUFA on endothelial function and inflammatory markers. Seventy patients with stable PAD classified as Rutherford stage 2 or 3 and good control of cardiovascular factors were randomised to receive either 4 g n-3 PUFA or placebo daily for 3 months in a double-blind fashion. Primary endpoint was endothelial function assessed by flow-mediated vasodilation (FMD). In addition, ankle–brachial index, maximum and pain-free walking distances were determined. Lipid parameters including the omega-3 index reflecting n-3 PUFA intake as well as pro-inflammatory, endothelial and platelet activation markers were measured over the same time interval. After 3 months of treatment with 4 g n-3 PUFA daily, a significant improvement of FMD was observed compared with placebo (n-3 PUFA, median Δ 3·7 (interquartile range (IQR) –1·8, 7·1) % v. placebo, Δ –0·5 (IQR –6·5, 3·0) %, P = 0·01 between the groups). After a 3-month washout period, this benefit was not sustained (n-3 PUFA, median Δ 0·6 (IQR –2·2, 5·6) % v. placebo, Δ –0·9 (IQR –6·6, 6·7) %, P = 0·20). In response to n-3 PUFA, an improvement of lipid parameters with a pronounced increase in the omega-3 index was seen. No changes were found for other parameters. In conclusion, in patients with PAD, 4 g/d n-3 PUFA improved cardiovascular risk in PAD patients, which needs testing in large-scale trials.

Increased attention has been paid to circadian patterns and how predisposition to metabolic disorders can be affected by meal timing. Currently, it is not clear which role can be attributed to the foods selected at meals. On a cross-sectional sub-cohort study (815 adults) within the European Prospective Investigation into Cancer and Nutrition-Potsdam study, we investigated whether the same foods (vegetables, fruits, refined grains, whole grains, red and processed meats) eaten at different meals (breakfast, lunch or dinner) show different associations with biomarkers of cardiometabolic risk. Meal-specific usual intakes were calculated from multiple 24-h dietary recalls. Multivariable-adjusted linear regression models showed that intake of vegetables at breakfast was associated with lower LDL-cholesterol (−0·37 mmol/l per 50 g; 95 % CI −0·61, −0·12) and vegetables at dinner was associated with higher HDL-cholesterol (0·05 mmol/l per 50 g; 95 % CI 0, 0·10). Fruit intake at breakfast was associated with lower glycated Hb (HbA1c) (−0·06 % per 50 g; 95 % CI −0·10, −0·01) and fruits at dinner with lower C-reactive protein (CRP) (−0·21 mg/l per 50 g; 95 % CI −0·42, −0·01). Red and processed meat intake at breakfast was associated with higher HbA1c (0·25 % per 50 g; 95 % CI 0·05, 0·46) and CRP (0·76 mg/l per 50 g; 95 % CI 0·15, 1·36). Our results suggest that by preferring fruits and vegetables and avoiding red and processed meats at specific meals (i.e. breakfast and dinner), cardiometabolic profiles and ultimately chronic disease risk could be improved. Lunch seemed to be a less important meal in terms of food–biomarker associations.