The cumulative effects of dietary arginine, leucine and protein levels on fat content, fatty acid composition and mRNA levels of genes controlling lipid metabolism in pig longissimus lumborum muscle and subcutaneous adipose tissue (SAT) were investigated. The experiment was performed on fifty-four intact male pigs (Duroc × Pietrain × Large White × Landrace crossbred), with a live weight ranging from 59 to 92 kg. The pigs were randomly assigned to one of six experimental treatments (n 9). The treatments followed a 2 × 3 factorial arrangement, with two levels of arginine supplementation (0 v. 1 %) and three levels of a basal diet (normal protein diet, NPD; reduced protein diet, RPD; reduced protein diet to achieve 2 % of leucine, RPDL). The results showed that dietary arginine supplementation did not affect the intramuscular fat (IMF) content and back fat thickness, but increased the total fat in SAT. This effect was associated with an increase in fatty acid synthase (FASN) and stearoyl-CoA desaturase (SCD) mRNA levels in SAT, which suggests that arginine might be involved in the differential regulation of some key lipogenic genes in pig muscle and SAT. The increase in IMF content under the RPD, with or without leucine supplementation, was accompanied by increased FASN and SCD mRNA levels. Arginine supplementation did not influence the percentage of main fatty acids, while the RPD had a significant effect on fatty acid composition in both tissues. Leucine supplementation of RPD did not change IMF, total fat of SAT and back fat thickness, but increased 16 : 0 and 18 : 1cis-9 and decreased 18 : 2n-6 in muscle.

n-3 PUFA are crucial for health and development. Their effects as regulators of lipid and glucose metabolism are well documented. They also appear to affect protein metabolism, especially by acting on insulin sensitivity. The aim of the present study was to investigate the role of n-3 PUFA, i.e. the precursor α-linolenic acid (ALA) 18 : 3n-3 or long-chain PUFA (LC-PUFA), in chickens, by focusing on their potential function as co-regulators of the insulin anabolic signalling cascade. Ross male broilers were divided into six dietary treatment groups. Diets were isoproteic (22 % crude protein) and isoenergetic (12·54 MJ metabolisable energy/kg) and contained similar lipid levels (6 %) provided by different proportions of various lipid sources: oleic sunflower oil rich in 18 : 1n-9 as control; fish oil rich in LC-PUFA; rapeseed and linseed oils providing ALA. The provision of diets enriched with n-3 PUFA, i.e. rich in LC-PUFA or in the precursor ALA, for 3 weeks improved the growth performance of chickens, whereas that of only the ALA diet enhanced the development of the pectoralis major muscle. At 23 d of age, we studied the insulin sensitivity of the pectoralis major muscle and liver of chickens after an intravenous injection of insulin or saline. The present results indicate that the activation patterns of n-3 PUFA are different in the liver and muscles. An ALA-enriched diet may improve insulin sensitivity in muscles, with greater activation of the insulin-induced 70 kDa ribosomal protein S6 kinase/ribosomal protein S6 pathway involved in the translation of mRNA into proteins, thereby potentially increasing muscle protein synthesis and growth. Our findings provide a basis on which to optimise dietary fatty acid provision in growing animals.

The aim of the present systematic review and meta-analysis was to examine the long-term effects ( ≥ 12 months) of high-fat (HF) v. low-fat (LF) diet consumption on the indicators of glycaemic control as well as cardiovascular risk factors in pre-diabetic and diabetic individuals. Literature search was carried out using the electronic databases MEDLINE, Embase and the Cochrane Trial Register until November 2013. Study-specific weighted mean differences (MD) were pooled using a random-effects model of the Cochrane software package Review Manager 5.1 and Stata 12.0 was used for meta-regressions. A total of fourteen trials met the inclusion criteria and a maximum of 1753 subjects were included in the meta-analysis. HF regimens were found to result in a significant decrease in TAG levels (MD − 0·19 mmol/l, 95 % CI − 0·23, − 0·14, P< 0·001; I2= 0 %, P= 0·58) and diastolic blood pressure (MD − 1·30 mmHg, 95 % CI − 1·73, − 0·87, P< 0·001; I2= 0 %, P= 0·60) and a significant increase in HDL-cholesterol levels (MD 0·05 mmol/l, 95 % CI 0·01, 0·08, P= 0·01; I2= 57 %, P= 0·01). In addition, MD in the reductions of fasting glucose levels ( − 0·41 mmol/l, 95 % CI − 0·74, − 0·08, P= 0·01; I2= 56 %, P= 0·02) were significantly high in patients with type 2 diabetes adhering to a HF diet. HF and LF diets might not be of equal value in the management of either pre-diabetes or type 2 diabetes, leading to emphasis being placed on the recommendations of HF diets.

The present systematic review examined the relationship between nutrition knowledge and dietary intake in adults (mean age ≥ 18 years). Relevant databases were searched from the earliest record until November 2012. Search terms included: nutrition; diet or food knowledge and energy intake; feeding behaviour; diet; eating; nutrient or food intake or consumption. Included studies were original research articles that used instruments providing quantitative assessment of both nutrition knowledge and dietary intake and their statistical association. The initial search netted 1 193 393 potentially relevant articles, of which twenty-nine were eligible for inclusion. Most of them were conducted in community populations (n 22) with fewer (n 7) in athletic populations. Due to the heterogeneity of methods used to assess nutrition knowledge and dietary intake, a meta-analysis was not possible. The majority of the studies (65·5 %: community 63·6 %; athletic 71·4 %) reported significant, positive, but weak (r< 0·5) associations between higher nutrition knowledge and dietary intake, most often a higher intake of fruit and vegetables. However, study quality ranged widely and participant representation from lower socio-economic status was limited, with most participants being tertiary educated and female. Well-designed studies using validated methodologies are needed to clarify the relationship between nutrition knowledge and dietary intake. Diet quality scores or indices that aim to evaluate compliance to dietary guidelines may be particularly valuable for assessing the relationship between nutrition knowledge and dietary intake. Nutrition knowledge is an integral component of health literacy and as low health literacy is associated with poor health outcomes, contemporary, high-quality research is needed to inform community nutrition education and public health policy.

Observational studies have suggested that the intake of flavonoids is associated with a decreased risk of CVD. However, the results of these studies remain controversial. The aim of the present study was to evaluate the association between dietary flavonoid intake and CVD risk by conducting a systematic review of prospective cohort studies. Electronic reference databases were searched to identify studies that met the pre-stated inclusion criteria. The studies were assessed for eligibility and data were extracted by two authors independently. For each study, relative risks (RR) and 95 % CI were extracted and pooled using either a fixed-effects or a random-effects model. Generalised least-squares trend estimation analysis was used to evaluate dose–response relationships. The inclusion criteria were met by fourteen prospective cohort studies. The intakes of anthocyanidins (RR 0·89, 95 % CI 0·83, 0·96), proanthocyanidins (RR 0·90, 95 % CI 0·82, 0·98), flavones (RR 0·88, 95 % CI 0·82, 0·96), flavanones (RR 0·88, 95 % CI 0·82, 0·96) and flavan-3-ols (RR 0·87, 95 % CI 0·80, 0·95) were inversely associated with the risk of CVD when comparing the highest and lowest categories of intake. A similar association was observed for flavonol intake and CVD risk. Sensitivity and subgroup analyses further supported this association. The summary RR for CVD for every 10 mg/d increment in flavonol intake was 0·95 (95 % CI 0·91, 0·99). The present systematic review suggests that the dietary intakes of six classes of flavonoids, namely flavonols, anthocyanidins, proanthocyanidins, flavones, flavanones and flavan-3-ols, significantly decrease the risk of CVD.

Tea consumption has inconsistently been shown to be associated with the risk of type 2 diabetes (T2D). The aim of the present study was to conduct a dose–response meta-analysis of cohort studies assessing the association between consumption of tea and risk of developing T2D. Pertinent studies were identified by searching PubMed, Web of Science and EMBASE through 31 March 2013. A total of sixteen cohorts from fifteen articles that reported 37 445 cases of diabetes among 545 517 participants were included. A significant linearly inverse association between tea consumption and T2D risk was found (P for linear trend = 0·02). An increase of 2 cups/d in tea consumption was found to be associated with a 4·6 (95 % CI 0·9, 8·1) % reduced risk of T2D. On the basis of the dose–response meta-analysis, the predicted relative risks of diabetes for 0, 1, 2, 3, 4, 5 and 6 cups of tea consumed per d were 1·00 (referent), 0·97 (95 % CI 0·94, 1·01), 0·95(95 % CI 0·92, 0·98), 0·93 (95 % CI 0·88, 0·98), 0·90 (95 % CI 0·85, 0·96), 0·88 (95 % CI 0·83, 0·93) and 0·85 (95 % CI 0·80, 0·91), respectively. There was a statistically significant heterogeneity within the selected studies (Q= 45·32, P< 0·001, I2= 60·3 %). No evidence of substantial small-study bias was found (P= 0·46). Our findings suggest that tea consumption could be linearly inversely associated with T2D risk. Future well-designed observational studies that account for different characteristics of tea such as tea types, preparation methods and tea strength are needed to fully characterise such an association.

Different dietary fat and energy subtypes have an impact on both the metabolic health and the intestinal microbiota population of the host. The present study assessed the impact of dietary fat quality, with a focus on dietary fatty acid compositions of varying saturation, on the metabolic health status and the intestinal microbiota composition of the host. C57BL/6J mice (n 9–10 mice per group) were fed high-fat (HF) diets containing either (1) palm oil, (2) olive oil, (3) safflower oil or (4) flaxseed/fish oil for 16 weeks and compared with mice fed low-fat (LF) diets supplemented with either high maize starch or high sucrose. Tissue fatty acid compositions were assessed by GLC, and the impact of the diet on host intestinal microbiota populations was investigated using high-throughput 16S rRNA sequencing. Compositional sequencing analysis revealed that dietary palm oil supplementation resulted in significantly lower populations of Bacteroidetes at the phylum level compared with dietary olive oil supplementation (P< 0·05). Dietary supplementation with olive oil was associated with an increase in the population of the family Bacteroidaceae compared with dietary supplementation of palm oil, flaxseed/fish oil and high sucrose (P< 0·05). Ingestion of the HF-flaxseed/fish oil diet for 16 weeks led to significantly increased tissue concentrations of EPA, docosapentaenoic acid and DHA compared with ingestion of all the other diets (P< 0·05); furthermore, the diet significantly increased the intestinal population of Bifidobacterium at the genus level compared with the LF-high-maize starch diet (P< 0·05). These data indicate that both the quantity and quality of fat have an impact on host physiology with further downstream alterations to the intestinal microbiota population, with a HF diet supplemented with flaxseed/fish oil positively shaping the host microbial ecosystem.

Creatine is an important molecule involved in cellular energy metabolism. Creatine is spontaneously converted to creatinine at a rate of 1·7 % per d; creatinine is lost in the urine. Creatine can be obtained from the diet or synthesised from endogenous amino acids via the enzymes arginine:glycine amidinotransferase (AGAT) and guanidinoacetate N-methyltransferase (GAMT). The liver has high GAMT activity and the kidney has high AGAT activity. Although the pancreas has both AGAT and GAMT activities, its possible role in creatine synthesis has not been characterised. In the present study, we examined the enzymes involved in creatine synthesis in the pancreas as well as the synthesis of guanidinoacetate (GAA) and creatine by isolated pancreatic acini. We found significant AGAT activity and somewhat lower GAMT activity in the pancreas and that pancreatic acini had measurable activities of both AGAT and GAMT and the capacity to synthesise GAA and creatine from amino acids. Creatine supplementation led to a decrease in AGAT activity in the pancreas, though it did not affect its mRNA or protein abundance. This was in contrast with the reduction of AGAT activity and mRNA and protein abundance in the kidney, suggesting that the regulatory mechanisms that control the expression of this enzyme in the pancreas are different from those in the kidney. Dietary creatine increased the concentrations of GAA, creatine and phosphocreatine in the pancreas. Unexpectedly, creatine supplementation decreased the concentrations of S-adenosylmethionine, while those of S-adenosylhomocysteine were not altered significantly.

The present study aimed to investigate the effect of dietary actinidin on the kinetics of gastric digestion of beef muscle proteins and on the rate of stomach emptying in growing pigs. For this purpose, 120 pigs (mean body weight 28 (sd 2·9) kg) were fed beef muscle protein-based diets containing either actinidin (fresh green kiwifruit pulp or gold kiwifruit pulp supplemented with purified actinidin) or no actinidin (fresh gold kiwifruit pulp or green kiwifruit pulp with inactivated actinidin). Additionally, fifteen pigs were fed with a protein-free diet to determine the endogenous protein flow. Pigs were euthanised at exactly 0·5, 1, 3, 5 and 7 h postprandially (n 6 per time point for each kiwifruit diet and n 3 for protein-free diet). Stomach chyme was collected for measuring gastric retention, actinidin activity, individual beef muscle protein digestion based on SDS–PAGE and the degree of hydrolysis based on the appearance of free amino groups. The stomach emptying of DM and N was faster when actinidin was present in the diet (P< 0·05): the half gastric emptying time of DM was 137 v. 172 min ( ± 7·4 min pooled standard error) for the diets with and without actinidin, respectively. The presence of dietary actinidin in the stomach chyme increased the digestion of beef muscle protein (P< 0·05) and, more specifically, those proteins with a high molecular weight (>34 kDa; P< 0·05). In conclusion, dietary actinidin fed in the form of fresh green kiwifruit increased the rate of gastric emptying and the digestion of several beef muscle proteins.

The gut microbiota plays an important role in the development of the immune and gastrointestinal systems of infants. In the present study, we investigated whether increased salmon consumption during pregnancy, maternal weight gain during pregnancy or mode of infant feeding alter the markers of gut immune defence and inflammation. Women (n 123) who rarely ate oily fish were randomly assigned to continue consuming their habitual diet or to consume two 150 g portions of farmed salmon per week from 20 weeks of pregnancy to delivery. Faecal samples were collected from the mothers (n 75) at 38 weeks of gestation and from their infants (n 38) on days 7, 14, 28 and 84 post-partum. Fluorescence in situ hybridisation was used to determine faecal microbiota composition and ELISA to measure faecal secretory IgA (sIgA) and calprotectin concentrations. There was no effect of salmon consumption on maternal faecal microbiota or on maternal or infant faecal sIgA and calprotectin concentrations. The degree of weight gain influenced maternal faecal microbiota, and the mode of infant feeding influenced infant faecal microbiota. Faecal samples collected from infants in the salmon group tended to have lower bacterial counts of the Atopobium cluster compared with those collected from infants in the control group (P= 0·097). This difference was significant in the formula-fed infants (P< 0·05), but not in the exclusively breast-fed infants. In conclusion, the impact of oily fish consumption during pregnancy on maternal and infant gut microbiota composition is limited, but significant differences are associated with maternal weight gain during pregnancy and mode of infant feeding.

Several studies using different animal models have demonstrated that the consumption of soya protein (SP) reduces serum cholesterol concentrations by increasing the excretion of bile acids (BA). However, the mechanism by which SP enhances BA excretion is not fully understood. Therefore, the aim of the present study was to determine whether the consumption of SP regulates the expression of key enzymes involved in hepatic BA synthesis and the transporters involved in reverse cholesterol transport (RCT) via fibroblast growth factor 15 (FGF15) and/or small heterodimer protein (SHP) in rats. To achieve this aim, four groups of rats were fed experimental diets containing 20 % casein (C) or SP with or without the addition of 0·2 % cholesterol and the expression of hepatic genes involved in BA synthesis and the ileal and hepatic RCT was measured. Rats fed the SP diet had higher concentrations of ileal FGF15 and hepatic FGF15 receptor (FGFR4) and increased expression of SHP and liver receptor homolog 1 (LRH1) than those fed the C diet; as a result, the excretion of faecal BA was greater. The addition of cholesterol to the diet repressed the protein abundance of FGF15 and FGFR4; however, SP increased the expression of SHP and LRH1 to a lesser extent. Nonetheless, the expression of ABCG5/8 was increased in the intestine of rats fed the SP diet, and the effect was enhanced by the addition of cholesterol to the diet. In conclusion, SP in the presence of cholesterol increases BA synthesis via the repressions of FGF15 and SHP and accelerates BA excretion to prevent cholesterol overload in the enterocytes by increasing RCT.

The intestinal immune system maintains a delicate balance between immunogenicity against invading pathogens and tolerance to the commensal microbiota and food antigens. Different strains of probiotics possess the ability to finely regulate the activation of dendritic cells (DC), polarising the subsequent activity of T-cells. Nevertheless, information about their underlying mechanisms of action is scarce. In the present study, we investigated the immunomodulatory effects of a potentially probiotic strain, Lactobacillus rhamnosus CNCM I-4036, and its cell-free culture supernatant (CFS) on human DC challenged with Escherichia coli. The results showed that the levels of pro-inflammatory cytokines such as IL-1β, IL-6, IL-8 and IL-12p70 were higher in the cells treated with live L. rhamnosus than in the cells treated with the CFS. In the presence of E. coli, the supernatant was more effective than the probiotic bacteria in reducing the secretion of pro-inflammatory cytokines. In addition, live L. rhamnosus potently induced the production of transforming growth factor (TGF)-β1 and TGF-β2, whereas the CFS increased the secretion of TGF-β1. However, in the presence of E. coli, both treatments restored the levels of TGF-β. The probiotic strain L. rhamnosus CNCM I-4036 and its CFS were able to activate the Toll-like receptor signalling pathway, enhancing innate immunity. The two treatments induced gene transcription of TLR-9. Live L. rhamnosus activated the expression of TLR-2 and TLR-4 genes, whereas the CFS increased the expression of TLR-1 and TLR-5 genes. In response to the stimulation with probiotic/CFS and E. coli, the expression of each gene tested was notably increased, with the exception of TNF-α and NFKBIA. In conclusion, the CFS exhibited an extraordinary ability to suppress the production of pro-inflammatory cytokines by DC, and may be used as an effective and safer alternative to live bacteria.

The aim of using oral and sublingual immunotherapy with food allergies is to enable the safe consumption of foods containing these allergens in patients with food allergies. In the present study, a systematic review of intervention studies was undertaken; this involved the searching of eleven international databases for controlled clinical trials. We identified 1152 potentially relevant papers, from which we selected twenty-two reports of twenty-one eligible trials (i.e. eighteen randomised controlled trials and three controlled clinical trials). The meta-analysis revealed a substantially lower risk of reactions to the relevant food allergen in those receiving orally administered immunotherapy (risk ratios (RR) 0·21, 95 % CI 0·12, 0·38). The meta-analysis of immunological data demonstrated that skin prick test responses to the relevant food allergen significantly decreased with immunotherapy (mean difference − 2·96 mm, 95 % CI − 4·48, − 1·45), while allergen-specific IgG4 levels increased by an average of 19·9 (95 % CI 17·1, 22·6) μg/ml. Sensitivity analyses excluding studies at the highest risk of bias and subgroup analyses in relation to specific food allergens and treatment approaches generated comparable summary estimates of effectiveness and immunological changes. Pooling of the safety data revealed an increased risk of local (i.e. minor oropharyngeal/gastrointestinal) adverse reactions with immunotherapy (RR 1·47, 95 % CI 1·11, 1·95); there was a non-significant increased average risk of systemic adverse reactions with immunotherapy (RR 1·08, 95 % CI 0·97, 1·19). There is strong evidence that orally administered immunotherapy can induce immunomodulatory changes and thereby promote desensitisation to a range of foods. However, given the paucity of evidence on longer-term safety, effectiveness and cost-effectiveness, orally administered immunotherapy should not be used outside experimental conditions presently.

It is becoming evident that nutrients and metabolic intermediates derived from such nutrients regulate cellular function by activating a number of cell-surface G-protein coupled receptors (GPCRs). Until now, members of the GPCR family have largely been considered as the molecular targets that communicate cellular signals initiated by hormones and neurotransmitters. Recently, based on tissue expression patterns of these receptors and the concept that they may elicit the production of a range of appetite- and hunger-regulating peptides, such nutrient sensing GPCRs are attracting considerable attention due to their potential to modulate satiety, improve glucose homeostasis and supress the production of various pro-inflammatory mediators. Despite the developing interests in these nutrients sensing GPCR both as sensors of nutritional status, and targets for limiting the development of metabolic diseases, major challenges remain to exploit their potential for therapeutic purposes. Mostly, this is due to limited characterisation and validation of these receptors because of paucity of selective and high-potency/affinity pharmacological agents to define the detailed function and regulation of these receptors. However, ongoing clinical trials of agonists of free fatty acid receptor 1 suggest that this receptor and other receptors for free fatty acids may provide a successful strategy for controlling hyperglycaemia and providing novel approaches to treat diabetes. Receptors responsive to free fatty acid have been of particular interest, and some aspects of these are considered herein.