Ingestion of collagen peptide (CP) elicits beneficial effects on the body, including improvement in blood lipid profiles, but the underlying mechanisms remain unclear. The purpose of this study was to investigate the effects of CP ingestion on the liver, which controls lipid metabolism in the body. Male BALB/cCrSlc mice were bred with the AIN-93M diet containing 14 % casein or the AIN-93M-based low-protein diet containing 10 % casein or a diet containing 6 % casein+4 % CP for 10 weeks (n 12/group). Total, free and esterified cholesterol levels in the blood decreased in the CP group. DNA microarray analysis of the liver revealed that expressions of genes related to lipid metabolic processes such as the PPAR signalling pathway and fatty acid metabolism increased in the CP group compared with the 10 % casein group. The expressions of several genes involved in steroid metabolic process, including Cyp7a1 and Cyp8b1, were decreased, despite being targets of transcriptional regulation by PPAR. These data suggest that lipid metabolism in the liver is altered by CP ingestion, and the decrease in blood cholesterol levels in the CP group is not due to enhancement of the steroid metabolic process. On the other hand, expressions of genes related to the unfolded protein response (UPR) significantly decreased at the mRNA level, suggesting that CP ingestion lowers endoplasmic reticulum stress. Indeed, protein levels of phosphorylated inositol-requiring enzyme 1 decreased after CP ingestion. Taken together, CP affects the broader pathways in the liver – not only lipid metabolism but also UPR.

The present study aimed to investigate the effects of maternal dietary butyrate supplementation on energy metabolism and mitochondrial biogenesis in offspring skeletal muscle and the possible mediating mechanisms. Virgin female rats were randomly assigned to either control or butyrate diets (1 % butyrate sodium) throughout gestation and lactation. At the end of lactation (21 d), the offspring were killed by exsanguination from the abdominal aorta under anaesthesia. The results showed that maternal butyrate supplementation throughout gestation and lactation did not affect offspring body weight. However, the protein expressions of G-protein-coupled receptors (GPR) 43 and 41 were significantly enhanced in offspring skeletal muscle of the maternal butyrate-supplemented group. The ATP content, most of mitochondrial DNA-encoded gene expressions, the cytochrome c oxidase subunit 1 and 4 protein contents and the mitochondrial DNA copy number were significantly higher in the butyrate group than in the control group. Meanwhile, the protein expressions of type 1 myosin heavy chain, mitochondrial transcription factor A, PPAR-coactivator-1α (PGC-1α) and uncoupling protein 3 were significantly increased in the gastrocnemius muscle of the treatment group compared with the control group. These results indicate for the first time that maternal butyrate supplementation during the gestation and lactation periods influenced energy metabolism and mitochondrial biogenesis through the GPR and PGC-1α pathways in offspring skeletal muscle at weaning.

Diets enriched with advanced glycation end products (AGE) have recently been related to muscle dysfunction processes. However, it remains unclear whether long-term exposure to an AGE-enriched diet impacts physiological characteristics of skeletal muscles. Therefore, we explored the differences in skeletal muscle mass, contractile function and molecular responses between mice receiving a diet high in AGE (H-AGE) and low in AGE (L-AGE) for 16 weeks. There were no significant differences between L-AGE and H-AGE mice with regard to body weight, food intake or epididymal fat pad weight. However, extensor digitorum longus (EDL) and plantaris (PLA) muscle weights in H-AGE mice were lower compared with L-AGE mice. Higher levels of Nε-(carboxymethyl)-l-lysine, a marker for AGE, in EDL muscles of H-AGE mice were observed compared with L-AGE mice. H-AGE mice showed lower muscle strength and endurance in vivo and lower muscle force production of PLA muscle in vitro. mRNA expression levels of myogenic factors including myogenic factor 5 and myogenic differentiation in EDL muscle were lower in H-AGE mice compared with L-AGE mice. The phosphorylation status of 70-kDa ribosomal protein S6 kinase Thr389, an indicator of protein synthesis signalling, was lower in EDL muscle of H-AGE mice than that of L-AGE mice. These findings suggest that long-term exposure to an AGE-enriched diet impairs skeletal muscle growth and muscle contractile function, and that these muscle dysfunctions may be attributed to the inhibition of myogenic potential and protein synthesis.

Farmed salmon feeds have changed from purely marine-based diets with high levels of EPA and DHA in the 1990s to the current 70 % plant-based diets with low levels of these fatty acids (FA). The aim of this study was to establish the impacts of low dietary EPA and DHA levels on performance and tissue integrity of Atlantic salmon (Salmo salar). Atlantic salmon (50 g) in seawater were fed fourteen experimental diets, containing five levels (0, 0·5, 1·0, 1·5 and 2·0 %) of EPA, DHA or a 1:1 EPA+DHA plus control close to a commercial diet, to a final weight of 400 g. Lack of EPA and DHA did not influence mortality, but the n-3-deficient group exhibited moderately slower growth than those fed levels above 0·5 %. The heart and brain conserved EPA and DHA levels better than skeletal muscle, liver, skin and intestine. Decreased EPA and DHA favoured deposition of pro-inflammatory 20 : 4n-6 and 20 : 3n-6 FA in membrane phospholipids in all tissues. When DHA was excluded from diets, 18 : 3n-3 and EPA were to a large extent converted to DHA. Liver, skeletal and cardiac muscle morphology was normal in all groups, with the exception of cytoplasm packed with large or foamy vacuoles and sometimes swollen enterocytes of intestine in both deficient and EPA groups. DHA supplementation supported normal intestinal structure, and 2·0 % EPA+DHA alleviated deficiency symptoms. Thus, EPA and DHA dietary requirements cannot be based exclusively on growth; tissue integrity and fish health also need to be considered.

Obesity is undoubtedly caused by a chronic positive energy balance. However, the early metabolic and hormonal responses to overeating are poorly described. This study determined glycaemic control and selected gut hormone responses to nutrient intake before and after 7 d of high-fat overfeeding. Nine healthy individuals (five males, four females) performed a mixed meal tolerance test (MTT) before and after consuming a high-fat (65 %), high-energy (+50 %) diet for 7 d. Measurements of plasma glucose, NEFA, acylated ghrelin, glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP) and serum insulin were taken before (fasting) and at 30-min intervals throughout the 180-min MTT (postprandial). Body mass increased by 0·79 (sem 0·14) kg after high-fat overfeeding (P<0·0001), and BMI increased by 0·27 (sem 0·05) kg/m2 (P=0·002). High-fat overfeeding also resulted in an 11·6 % increase in postprandial glucose AUC (P=0·007) and a 25·9 % increase in postprandial insulin AUC (P=0·005). Acylated ghrelin, GLP-1 and GIP responses to the MTT were all unaffected by the high-fat, high-energy diet. These findings demonstrate that even brief periods of overeating are sufficient to disrupt glycaemic control. However, as the postprandial orexigenic (ghrelin) and anorexigenic/insulintropic (GLP-1 and GIP) hormone responses were unaffected by the diet intervention, it appears that these hormones are resistant to short-term changes in energy balance, and that they do not play a role in the rapid reduction in glycaemic control.

Dietary cholesterol and plant sterols differentially modulate cholesterol kinetics and circulating cholesterol. Understanding how healthy individuals with their inherent variabilities in cholesterol trafficking respond to such dietary sterols will aid in improving strategies for effective cholesterol lowering and alleviation of CVD risk. The objectives of this study were to assess plasma lipid responsiveness to dietary cholesterol v. plant sterol consumption, and to determine the response in rates of cholesterol absorption and synthesis to each sterol using stable isotope approaches in healthy individuals. A randomised, double-blinded, crossover, placebo-controlled clinical trial (n 49) with three treatment phases of 4-week duration were conducted in a Manitoba Hutterite population. During each phase, participants consumed one of the three treatments as a milkshake containing 600 mg/d dietary cholesterol, 2 g/d plant sterols or a control after breakfast meal. Plasma lipid profile was determined and cholesterol absorption and synthesis were measured by oral administration of [3, 4-13C] cholesterol and 2H-labelled water, respectively. Dietary cholesterol consumption increased total (0·16 (sem 0·06) mmol/l, P=0·0179) and HDL-cholesterol (0·08 (sem 0·03) mmol/l, P=0·0216) concentrations with no changes in cholesterol absorption or synthesis. Plant sterol consumption failed to reduce LDL-cholesterol concentrations despite showing a reduction (6 %, P=0·0004) in cholesterol absorption. An over-compensatory reciprocal increase in cholesterol synthesis (36 %, P=0·0026) corresponding to a small reduction in absorption was observed with plant sterol consumption, possibly resulting in reduced LDL-cholesterol lowering efficacy of plant sterols. These data suggest that inter-individual variability in cholesterol trafficking mechanisms may profoundly impact plasma lipid responses to dietary sterols in healthy individuals.

The present study investigated the effects of dietary vitamin A on immune function in the proximal intestine (PI), mid intestine (MI) and distal intestine (DI) of young grass carp (Ctenopharyngodon idella). Fish were fed graded levels of dietary vitamin A for 10 weeks, and then a challenge test using an injection of Aeromonas hydrophila was conducted for 14 d. The results showed that, compared with the optimum vitamin A level, vitamin A deficiency significantly decreased fish growth performance, increased enteritis morbidity, decreased intestinal innate humoral immune response and aggravated intestinal inflammation. However, liver-expressed antimicrobial peptide 2A/B mRNA in the DI and IL-6, IL-17D, IL-10, transforming growth factor (TGF)-β1 and TGF-β2 mRNA in the PI were not affected by vitamin A levels. Meanwhile, vitamin A deficiency disturbed inflammatory cytokines in the PI, MI and DI, which might be partly linked to p38 mitogen-activated protein kinase (p38MAPK) signalling and NF-κB canonical signalling pathway (IκB kinase β (IKKβ), IKKγ, inhibitor of κBα, NF-κB p65 and c-Rel) rather than NF-κB non-canonical signalling pathway (NF-κB p52 and IKKα). However, the signalling molecules NF-κB p65 and p38MAPK did not participate in regulating cytokines in the PI. These results suggested that vitamin A deficiency decreased fish growth and impaired intestinal immune function, and that different immune responses in the PI, MI and DI were mediated partly by NF-κB canonical signalling and p38MAPK signalling pathways. On the basis of percentage of weight gain, to protect fish against enteritis morbidity and acid phosphatase activity, the optimum dietary vitamin A levels were estimated to be 0·664, 0·707 and 0·722 mg /kg, respectively.

Prebiotic supplementation modulates immune system development and function. However, less is known about the effects of maternal prebiotic consumption on offspring intestinal defences and immune system responsiveness. We investigated the effects of maternal short-chain fructo-oligosaccharide (scFOS) supplementation on mucin-secreting cells, ileal secretory IgA and cytokine secretion of weaned offspring and their humoral response to an oral vaccine against obligate intracellular Lawsonia intracellularis. Sows were fed a control diet (CTRL) or scFOS-supplemented diet during the last third of gestation and throughout lactation. At weaning, each litter was divided into two groups receiving a post-weaning CTRL or scFOS diet for a month. Pigs from the four groups were either non-vaccinated (n 16) or vaccinated (n 117) at day 33. Biomarkers related to intestinal defences and immune parameters were analysed 3 weeks later. SCFA production was assessed over time in suckling and weaned pigs. Maternal scFOS supplementation improved ileal cytokine secretions (interferon (IFN)-γ, P<0·05; IL-4, P=0·07) and tended to increase caecal goblet cell number (P=0·06). It increased IgA vaccine response in the serum (P<0·01) and ileal mucosa (P=0·08). Higher bacterial fermentative activity was observed during lactation (total faecal SCFA, P<0·001) and after weaning (colonic butyrate, P=0·10) in pigs from scFOS-supplemented mothers. No synergistic effect between maternal and post-weaning scFOS supplementation was observed. Therefore, maternal scFOS supplementation has long-lasting consequences by strengthening gut defences and immune response to a vaccine against an intestinal obligate intracellular pathogen. Prebiotic consumption by gestating and lactating mothers is decisive in modulating offspring intestinal immunity.

Intestinal barrier integrity is a prerequisite for homeostasis of mucosal function, which is balanced to maximise absorptive capacity, while maintaining efficient defensive reactions against chemical and microbial challenges. Evidence is mounting that disruption of epithelial barrier integrity is one of the major aetiological factors associated with several gastrointestinal diseases, including infection by pathogens, obesity and diabetes, necrotising enterocolitis, irritable bowel syndrome and inflammatory bowel disease. The notion that specific probiotic bacterial strains can affect barrier integrity fuelled research in which in vitro cell lines, animal models and clinical trials are used to assess whether probiotics can revert the diseased state back to homeostasis and health. This review catalogues and categorises the lines of evidence available in literature for the role of probiotics in epithelial integrity and, consequently, their beneficial effect for the reduction of gastrointestinal disease symptoms.

The macular carotenoids lutein (L), zeaxanthin (Z) and meso-zeaxanthin (MZ) accumulate at the macula, where they are collectively referred to as macular pigment (MP). Augmentation of this pigment, typically achieved through diet and supplementation, enhances visual function and protects against progression of age-related macular degeneration. However, it is known that eggs are a rich dietary source of L and Z, in a highly bioavailable matrix. In this single-blind placebo-controlled study, L- and MZ-enriched eggs and control non-enriched eggs were fed to human subjects (mean age 41 and 35 years, respectively) over an 8-week period, and outcome measures included MP, visual function and serum concentrations of carotenoids and cholesterol. Serum carotenoid concentrations increased significantly in control and enriched egg groups, but to a significantly greater extent in the enriched egg group (P<0·001 for L, Z and MZ). There was no significant increase in MP in either study group post intervention, and we saw no significant improvement in visual performance in either group. Total cholesterol increased significantly in each group, but it did not exceed the upper limit of the normative range (6·5 mmol/l). Therefore, carotenoid-enriched eggs may represent an effective dietary source of L, Z and MZ, reflected in significantly raised serum concentrations of these carotenoids, and consequentially improved bioavailability for capture by target tissues. However, benefits in terms of MP augmentation and /or improved visual performance were not realised over the 8-week study period, and a study of greater duration will be required to address these questions.

This study aimed to examine the association between vitamin B6, folate and vitamin B12 biomarkers and plasma fatty acids in European adolescents. A subsample from the Healthy Lifestyle in Europe by Nutrition in Adolescence study with valid data on B-vitamins and fatty acid blood parameters, and all the other covariates used in the analyses such as BMI, Diet Quality Index, education of the mother and physical activity assessed by a questionnaire, was selected resulting in 674 cases (43 % males). B-vitamin biomarkers were measured by chromatography and immunoassay and fatty acids by enzymatic analyses. Linear mixed models elucidated the association between B-vitamins and fatty acid blood parameters (changes in fatty acid profiles according to change in 10 units of vitamin B biomarkers). DHA, EPA) and n-3 fatty acids showed positive associations with B-vitamin biomarkers, mainly with those corresponding to folate and vitamin B12. Contrarily, negative associations were found with n-6:n-3 ratio, trans-fatty acids and oleic:stearic ratio. With total homocysteine (tHcy), all the associations found with these parameters were opposite (for instance, an increase of 10 nmol/l in red blood cell folate or holotranscobalamin in females produces an increase of 15·85 µmol/l of EPA (P value <0·01), whereas an increase of 10 nmol/l of tHcy in males produces a decrease of 2·06 µmol/l of DHA (P value <0·05). Positive associations between B-vitamins and specific fatty acids might suggest underlying mechanisms between B-vitamins and CVD and it is worth the attention of public health policies.

Education interventions that stimulate complementary feeding practices can improve the nutritional status of children and may protect against future chronic diseases. We assessed the long-term effectiveness of dietary intervention during the 1st year of life on insulin resistance levels, and investigated the relationship between insulin resistance and weight changes over time. A randomised field trial was conducted among 500 mothers who gave birth to full-term infants between October 2001 and June 2002 in a low-income area in São Leopoldo, Brazil. Mother–child pairs were randomly assigned to intervention (n 200) and control groups (n 300), and the mothers in the intervention group received dietary counselling on breast-feeding and complementary feeding of their children during the 1st year of life. Fieldworkers blinded to assignment assessed socio-demographic, dietary and anthropometric data during follow-up at ages 1, 4 and 8 years. Blood tests were performed in 305 children aged 8 years to measure fasting serum glucose and insulin concentrations and the homoeostasis model assessment index of insulin resistance (HOMA-IR). At the age of 8 years, the intervention group showed no changes in glucose and insulin concentrations or HOMA-IR values (change 0·07; 95 % CI −0·06, 0·21 for girls; and change −0·07; 95 % CI −0·19, 0·04 for boys) compared with study controls. Insulin resistance was highly correlated, however, with increases in BMI between birth and 8 years of age. Although this dietary intervention had no impact on glucose profile at age 8 years, our findings suggest that BMI changes in early childhood can serve as an effective marker of insulin resistance.

Malnutrition in institutionalised elderly increases morbidity and care costs. Meat and dairy foods are high-quality protein sources so adequate intakes may reduce malnutrition risk. We aimed to determine whether inadequate intakes of meat and dairy foods contribute to malnutrition in institutionalised elderly. This cross-sectional study involved 215 elderly residents (70·2 % females, mean age 85·8 years) from twenty-one aged-care facilities in Melbourne, Australia. Dietary intake was assessed using observed plate waste. Food groups and serving sizes were based on the Australian Guide to Healthy Eating. Nutrient content was analysed using a computerised nutrient analysis software (Xyris). Malnutrition risk was assessed using the Mini Nutrition Assessment (MNA) tool; a score between 24 and 30 indicates normal nutritional status. Data were analysed using robust regression. Mean MNA score was 21·6 (sd 2·7). In total, 68 % of residents were malnourished or at risk of malnutrition (MNA score≤23·5). Protein intake was 87 (sd 28) % of the Australian recommended dietary intake (RDI). Consumption averaged 1 serving each of dairy foods and meat daily. Number of dairy and meat servings related to proportion of protein RDI (both P<0·001), with the former contributing 13 % and the latter 12 % to protein RDI. Number of dairy servings (P<0·001), but not meat servings increased MNA score; each dairy serving was associated with a 1 point increase in MNA score so based on current intakes, on average if residents consumed the recommend four dairy servings (addition of 3 points to MNA score) they would achieve normal nutrition status (>24 points). Provision of meat and dairy foods did not meet recommended levels. On the basis of current dietary intakes in aged-care residents, increasing consumption of dairy foods to the recommended four servings daily ensures protein adequacy and may reduce malnutrition risk in institutionalised elderly, and so reduce risk of comorbidities and costs associated with malnutrition.

This cohort study examined the association between total and individual dairy products and the risk of developing the metabolic syndrome (MetS) and its components in Korean adults from the Korean Genome and Epidemiology Study. We prospectively analysed 5510 participants aged 40–69 years without the MetS at baseline during a 10-year follow-up period. Dairy consumption was assessed with a semi-quantitative FFQ at baseline and after 4 years. The MetS was defined according to the criteria by the National Cholesterol Education Program Adult Treatment Panel III. The Cox’s proportional hazard model was used to examine the association between consumption of total dairy products, milk and yogurt in servings per week and the risk of incident MetS or individual components. A total of 2103 subjects developed the MetS (38·2 %) during an average follow-up of 67·4 months (range 17–104 months). Frequent dairy consumption (>7 servings of total dairy and milk/week, ≥4 servings of yogurt/week) was associated with a reduced risk of incident MetS and its components. In the multivariable adjusted model, hazard ratios for the MetS were 0·51 (95 % CI 0·43, 0·61) for total dairy products, 0·50 (95 % CI 0·38, 0·66) for milk and 0·67 (95 % CI 0·57, 0·78) for yogurt in frequent consumers compared with non-consumers. An inverse association between milk/yogurt and low HDL-cholesterol was shown only in women. In conclusion, high consumption of individual dairy products including milk and yogurt as well as total dairy were associated with a reduced risk of incident MetS and individual components in Korean adults.

The associations of dietary energy density with dietary intake and obesity have been largely unexplored in non-Western populations. The present cross-sectional study examined the associations using data from the 2012 National Health and Nutrition Survey, Japan. Dietary intake was assessed using a 1-d semi-weighed dietary record in 15 618 Japanese adults aged ≥20 years. Mean dietary energy density (calculated on the basis of foods only) was 5·98 (sd 1·20) kJ/g in men and 5·72 (sd 1·16) kJ/g in women. Dietary energy density was positively associated with intakes of bread, noodles (only men), meat, fats and oils, and sugar and confectionery but inversely with intakes of white rice (only men), potatoes, pulses, vegetables, fruits, and fish and shellfish. For nutrient intake, dietary energy density was positively associated with total fat and SFA but inversely associated with all other nutrients examined such as protein, carbohydrate, alcohol (only women), dietary fibre, and several vitamins and minerals, including Na. After adjustment for potential confounding factors, dietary energy density was positively associated with abdominal obesity (waist circumference ≥80 cm) in women (adjusted prevalence ratio between the extreme tertiles 1·07; 95 % CI 1·02, 1·12; Pfor trend=0·003). Dietary energy density was also positively but non-significantly associated with general obesity (BMI≥25 kg/m2) in women (Pfor trend=0·08). There were no such associations in men. In conclusion, lower energy density of the diets of Japanese adults was associated with favourable food and nutrient intake patterns, except for higher Na, and, in only women, a lower prevalence of abdominal obesity.

I prophylaxis is the most effective strategy to eradicate I deficiency disorders, but it has been shown to affect the thyroid disease pattern. In this study, we assessed the frequency of thyroid disorders in an adult population living in two areas of southern Italy after implementing I prophylaxis. To this aim, a cross-sectional, population-based study including 489 subjects from an I-deficient rural and an I-sufficient urban area of southern Italy was conducted. Thyroid ultrasound was performed on all participants, and urine and blood samples were collected from each subject. The levels of thyroid-stimulating hormone (TSH), thyroglobulin (TgAb) and thyroperoxidase antibodies (TPOAb), urinary I excretion (UIE), and thyroid volume and echogenicity were evaluated. We found that the median UIE was higher in the urban than in the rural area (P=0·004), whereas the prevalence of subjects affected by goitre was higher in the rural compared with the urban area (P=0·003). Positive TgAb rather than TPOAb were more frequent in subjects from the urban area compared with the rural area (P=0·009). The hypoechoic pattern at thyroid ultrasound (HT-US) was similar between the two areas, but TgAb were significantly higher (P=0·01) in HT-US subjects from the urban area. The frequency of elevated TSH did not differ between the two screened populations, and no changes were found for TgAb positivity in subjects with high TSH in the urban compared with the rural area. Our findings support that the small risks of I supplementation are far outweighed by the substantial benefits of correcting I deficiency, although continued monitoring of populations is necessary.