It is unclear whether lifestyle modifications, such as dietary changes, should be advocated to prevent olfactory dysfunction. We investigated the association between dietary intakes of fats (saturated, mono-unsaturated and polyunsaturated fats, and cholesterol) and related food groups (nuts, fish, butter, margarine) with olfactory impairment. There were 1331 and 667 participants (older than 60 years) at baseline and 5-year follow-up, respectively, with complete olfaction and dietary data. Dietary data were collected using a validated semi-quantitative FFQ. Olfaction was measured using the San Diego Odor Identification Test. In a cross-sectional analysis of baseline data, those in the highest v. lowest quartile of n-6 PUFA intake had reduced odds of having any olfactory impairment, multivariable-adjusted OR 0·66 (95 % CI 0·44, 0·97), P for trend = 0·06. Participants in the highest v. lowest quartile of margarine consumption had a 65 % reduced odds of having moderate/severe olfactory impairment (P for trend = 0·02). Participants in the highest quartile compared to the lowest quartile (reference) of nut consumption had a 46 % (P for trend = 0·01) and 58 % (P for trend = 0·001) reduced odds of having any or mild olfactory impairment, respectively. Older adults in the highest v. lowest quartile of fish consumption had 35 % (P for trend = 0·03) and 50 % (P for trend = 0·01) reduced likelihood of having any or mild olfactory impairment, respectively. In longitudinal analyses, a marginally significant association was observed between nut consumption and incidence of any olfactory impairment, highest v. lowest quartile of nut consumption: OR 0·61 (95 % CI 0·37, 1·00). Older adults with the highest consumption of nuts and fish had reduced odds of olfactory impairment, independent of potential confounding variables.

This study was conducted to assess the effects of long-term Se administration on the regression and metabolic status of patients with cervical intraepithelial neoplasia grade 1 (CIN1). This randomised, double-blind, placebo-controlled trial was carried out among fifty-eight women diagnosed with CIN1. To diagnose CIN1, we used specific diagnostic procedures of biopsy, pathological diagnosis and colposcopy. Patients were randomly assigned to two groups to receive 200 μg Se supplements as Se yeast (n 28) or placebo (n 28) daily for 6 months. After 6 months of taking Se supplements, a greater percentage of women in the Se group had regressed CIN1 (88·0 v. 56·0 %; P=0·01) compared with those in the placebo group. Long-term Se supplementation, compared with the placebo, resulted in significant decreases in fasting plasma glucose levels (−0·37 (sd 0·32) v. +0·07 (sd 0·63) mmol/l; P=0·002), serum insulin levels (−28·8 (sd 31·2) v. +13·2 (sd 40·2) pmol/l; P<0·001), homeostatic model assessment of insulin resistance values (−1·3 (se 1·3) v. +0·5 (se 1·4); P<0·001) and a significant elevation in quantitative insulin sensitivity check index (+0·03 (sd 0·03) v. −0·01 (sd 0·01); P<0·001). In addition, patients who received Se supplements had significantly decreased serum TAG (−0·14 (sd 0·55) v. +0·15 (sd 0·38) mmol/l; P=0·02) and increased HDL-cholesterol levels (+0·13 (sd 0·21) v. −0·01 (sd 0·15) mmol/l; P=0·003). In addition, compared with the placebo group, there were significant rises in plasma total antioxidant capacity (+186·1 (sd 274·6) v. +42·8 (sd 180·4) mmol/l; P=0·02) and GSH levels (+65·0 (sd 359·8) v. −294·2 (sd 581·8) μmol/l; P=0·007) and a significant decrease in malondialdehyde levels (−1·5 (sd 2·1) v. +0·1 (sd 1·4) μmol/l; P=0·001) among those who took Se supplements. Overall, taking Se supplements among patients with CIN1 led to its regression and had beneficial effects on their metabolic profiles.

Administration of Lactobacillus gasseri SBT2055 (LG2055) has been shown to prevent body weight gain and it also down-regulates the expression of the Ccl2 gene in adipose tissue in diet-induced obese mice. The CC chemokine ligand 2 has a crucial role in macrophage infiltration into adipose tissue, which is known to exacerbate inflammation. However, it is not yet known how LG2055 affects the invasion of macrophages into adipose tissue. C57BL/6J male mice were fed a normal-fat diet (10 % energy fat), high-fat diet (HFD; 45 % energy fat), or HFD containing LG2055 for 12 weeks. After the feeding period, gene expression and macrophage population in adipose tissue were analysed by real-time PCR and flow cytometry, respectively. Body weight and abdominal fat weight were not altered by feeding LG2055. Flow cytometry analysis revealed that the population of macrophages in adipose tissue was significantly reduced by feeding LG2055 compared with HFD only. Furthermore, the ratio of classically activated inflammatory macrophages (M1 macrophages) to total macrophages was significantly decreased in the LG2055-fed group. The expressions of Ccl2, Ccr2 and Lep were down-regulated and that of Il6, Tnf and Nos2 tended to be down-regulated in adipose tissue by feeding LG2055. In addition, fasting glucose levels were significantly decreased in the LG2055-fed group. These data suggest that administration of LG2055 might attenuate inflammation, which is caused by the intake of an HFD, through the inhibition of macrophage invasion into adipose tissue.

The physico-chemical and interfacial properties of fat emulsions influence lipid digestion and may affect postprandial responses. The aim of the present study was to determine the effects of the modification of the interfacial layer of a fat emulsion by cross-linking on postprandial metabolic and appetite responses. A total of fifteen healthy individuals (26·5 (sem 6·9) years and BMI 21·9 (sem 2·0) kg/m2) participated in a cross-over design experiment in which they consumed two isoenergetic (1924 kJ (460 kcal)) and isovolumic (250 g) emulsions stabilised with either sodium caseinate (Cas) or transglutaminase-cross-linked sodium caseinate (Cas-TG) in a randomised order. Blood samples were collected from the individuals at baseline and for 6 h postprandially for the determination of serum TAG and plasma NEFA, cholecystokinin (CCK), glucagon-like peptide 1 (GLP-1), glucose and insulin responses. Appetite was assessed using visual analogue scales. Postprandial TAG and NEFA responses and gastric emptying (GE) rates were comparable between the emulsions. CCK increased more after the ingestion of Cas-TG than after the ingestion of Cas (P< 0·05), while GLP-1 responses did not differ between the two test emulsions. Glucose and insulin profiles were lower after consuming Cas-TG than after consuming Cas (P< 0·05). The overall insulin, glucose and CCK responses, expressed as areas above/under the curve, did not differ significantly between the Cas and Cas-TG meal conditions. Satiety ratings were reduced and hunger, desire to eat and thirst ratings increased more after the ingestion of Cas-TG than after the ingestion of Cas (P< 0·05). The present results suggest that even a subtle structural modification of the interfacial layer of a fat emulsion can alter the early postprandial profiles of glucose, insulin, CCK, appetite and satiety through decreased protein digestion without affecting significantly on GE or overall lipid digestion.

This prospective cohort study was conducted in eighteen Canadian hospitals with the aim of examining factors associated with nutritional decline in medical and surgical patients. Nutritional decline was defined based on subjective global assessment (SGA) performed at admission and discharge. Data were collected on demographics, medical information, food intake and patients’ satisfaction with nutrition care and meals during hospitalisation; 424 long-stay (≥7 d) patients were included; 38 % of them had surgery; 51 % were malnourished at admission (SGA B or C); 37 % had in-hospital changes in SGA; 19·6 % deteriorated (14·6 % from SGA A to B/C and 5 % from SGA B to C); 17·4 % improved (10·6 % from SGA B to A, 6·8 % from SGA C to B/A); and 63·0 % patients were stable (34·4 % were SGA A, 21·3 % SGA B, 7·3 % SGA C). One SGA C patient had weight loss ≥5 %, likely due to fluid loss and was designated as stable. A subset of 364 patients with admission SGA A and B was included in the multiple logistic regression models to determine factors associated with nutritional decline. After controlling for SGA at admission and the presence of a surgical procedure, lower admission BMI, cancer, two or more diagnostic categories, new in-hospital infection, reduced food intake, dissatisfaction with food quality and illness affecting food intake were factors significantly associated with nutritional decline in medical patients. For surgical patients, only male sex was associated with nutritional decline. Factors associated with nutritional decline are different in medical and surgical patients. Identifying these factors may assist nutritional care.

Evidence on the associations of dietary patterns with cognition in children is limited. Therefore, we investigated the associations of the Baltic Sea Diet Score (BSDS) and the Dietary Approaches to Stop Hypertension (DASH) score with cognition in children. The present cross-sectional study sample included 428 children aged 6–8 years (216 boys and 212 girls). The BSDS and the DASH score were calculated using data from 4 d food records, higher scores indicating better diet quality. Cognition was assessed by the Raven's Coloured Progressive Matrices (CPM) score, a higher score indicating better cognition. Among all children, the BSDS (standardised regression coefficient β = 0·122, P =0·012) and the DASH score (β = 0·121, P =0·015) were directly associated with the Raven's CPM score. Among boys, a lower BSDS (β = 0·244, P< 0·001) and a lower DASH score (β = 0·202, P= 0·003) were related to a lower Raven's CPM score. Boys in the lowest quartile of the BSDS (22·5 v. 25·3, P= 0·029) and the DASH score (22·4 v. 25·7, P= 0·008) had a lower Raven's CPM score than those in the highest quartile of the corresponding score. Among girls, the BSDS or the DASH score were not associated with cognition. In conclusion, a poorer diet quality was associated with worse cognition in children, and the relationship was stronger in boys than in girls.

Protein malnutrition promotes hepatic steatosis, decreases insulin-like growth factor (IGF)-I production and retards growth. To identify new molecules involved in such changes, we conducted DNA microarray analysis on liver samples from rats fed an isoenergetic low-protein diet for 8 h. We identified the fibroblast growth factor 21 gene (Fgf21) as one of the most strongly up-regulated genes under conditions of acute protein malnutrition (P<0·05, false-discovery rate<0·001). In addition, amino acid deprivation increased Fgf21 mRNA levels in rat liver-derived RL-34 cells (P<0·01). These results suggested that amino acid limitation directly increases Fgf21 expression. FGF21 is a polypeptide hormone that regulates glucose and lipid metabolism. FGF21 also promotes a growth hormone-resistance state and suppresses IGF-I in transgenic mice. Therefore, to determine further whether Fgf21 up-regulation causes hepatic steatosis and growth retardation after IGF-I decrease in protein malnutrition, we fed an isoenergetic low-protein diet to Fgf21-knockout (KO) mice. Fgf21-KO did not rescue growth retardation and reduced plasma IGF-I concentration in these mice. Fgf21-KO mice showed greater epididymal white adipose tissue weight and increased hepatic TAG and cholesterol levels under protein malnutrition conditions (P<0·05). Overall, the results showed that protein deprivation directly increased Fgf21 expression. However, growth retardation and decreased IGF-I were not mediated by increased FGF21 expression in protein malnutrition. Furthermore, FGF21 up-regulation rather appears to have a protective effect against obesity and hepatic steatosis in protein-malnourished animals.

The intestine requires a high amount of energy to maintain its health and function; thus, energy deficits in intestinal mucosa may lead to intestinal damage. Asparagine (Asn) is a precursor for many other amino acids such as aspartate, glutamine and glutamate, which can be used to supply energy to enterocytes. In the present study, we hypothesise that dietary supplementation of Asn could alleviate bacterial lipopolysaccharide (LPS)-induced intestinal injury via improvement of intestinal energy status. A total of twenty-four weaned piglets were assigned to one of four treatments: (1) non-challenged control; (2) LPS+0 % Asn; (3) LPS+0·5 % Asn; (4) LPS+1·0 % Asn. On day 19, piglets were injected with LPS or saline. At 24 h post-injection, piglets were slaughtered and intestinal samples were collected. Asn supplementation improved intestinal morphology, indicated by higher villus height and villus height:crypt depth ratio, and lower crypt depth. Asn supplementation also increased the ratios of RNA:DNA and protein:DNA as well as disaccharidase activities in intestinal mucosa. In addition, Asn supplementation attenuated bacterial LPS-induced intestinal energy deficits, indicated by increased ATP and adenylate energy charge levels, and decreased AMP:ATP ratio. Moreover, Asn administration increased the activities of key enzymes involved in the tricarboxylic acid cycle, including citrate synthase, isocitrate dehydrogenase and α-ketoglutarate dehydrogenase complex. Finally, Asn administration decreased the mRNA abundance of intestinal AMP-activated protein kinase-α1 (AMPKα1), AMPKα2, silent information regulator 1 (SIRT1) and PPARγ coactivator-1α (PGC1α), and reduced intestinal AMPKα phosphorylation. Collectively, these results indicate that Asn supplementation alleviates bacterial LPS-induced intestinal injury by modulating the AMPK signalling pathway and improving energy status.

The objective of the present study was to assess the impact of providing small-quantity lipid-based nutrient supplements (SQ-LNS) on the I status of young Burkinabe children. In total, thirty-four communities were assigned to intervention (IC) or non-intervention cohorts (NIC). IC children were randomly assigned to receive 20 g lipid-based nutrient supplements (LNS)/d containing 90 µg I with 0 or 10 mg Zn from 9 to 18 months of age, and NIC children received no SQ-LNS. All the children were exposed to iodised salt through the national salt iodization programme. Spot urinary iodine (UI), thyroid-stimulating hormone (TSH) and total thyroxine (T4) in dried blood spots as well as plasma thyroglobulin (Tg) concentrations were assessed at 9 and 18 months of age among 123 IC and fifty-six NIC children. At baseline and at 18 months, UI, TSH and T4 did not differ between cohorts. Tg concentration was higher in the NIC v. IC at baseline, but this difference did not persist at 18 months of age. In both cohorts combined, the geometric mean of UI was 339·2 (95 % CI 298·6, 385·2) µg/l, TSH 0·8 (95 % CI 0·7, 0·8) mU/l, T4 118 (95 % CI 114, 122) nmol/l and Tg 26·0 (95 % CI 24·3, 27·7) µg/l at 18 months of age. None of the children had elevated TSH at 18 months of age. Marginally more children in NIC (8·9 %) had low T4 (<65 nmol/l) compared with the IC (1·6 %) (P=0·052). Salt samples (n 106) were collected from randomly selected participants and assessed by titration for I content, which was on average 37 (sd 15) ppm (range 5–86 ppm); 95 % of households had adequately iodised salt (I>15 ppm). A reduction of SQ-LNS I content could be considered in settings with similarly successful salt iodisation programmes.

The aim of this study was to investigate the effects of the administration of oral arachidonic acid (AA) in rats with or without dextran sulphate sodium (DSS)-induced inflammatory bowel disease. Male Wistar rats were administered AA at 0, 5, 35 or 240 mg/kg daily by gavage for 8 weeks. Inflammatory bowel disease was induced by replacing drinking water with 3 % DSS solution during the last 7 d of the AA dosing period. These animals passed loose stools, diarrhoea and red-stained faeces. Cyclo-oxygenase-2 concentration and myeloperoxidase activity in the colonic tissue were significantly increased in the animals given AA at 240 mg/kg compared with the animals given AA at 0 mg/kg. Thromboxane B2 concentration in the medium of cultured colonic mucosae isolated from these groups was found to be dose-dependently increased by AA, and the increase was significant at 35 and 240 mg/kg. Leukotriene B4 concentration was also significantly increased and saturated at 5 mg/kg. In addition, AA at 240 mg/kg promoted DSS-induced colonic mucosal oedema with macrophage infiltration. In contrast, administration of AA for 8 weeks, even at 240 mg/kg, showed no effects on the normal rats. These results suggest that in rats with bowel disease AA metabolism is affected by oral AA, even at 5 mg/kg per d, and that excessive AA may aggravate inflammation, whereas AA shows no effects in rats without inflammatory bowel disease.

This study investigated the effect of a caffeinated energy drink on various aspects of performance in sprint swimmers. In a randomised and counterbalanced order, fourteen male sprint swimmers performed two acute experimental trials after the ingestion of a caffeinated energy drink (3 mg/kg) or after the ingestion of the same energy drink without caffeine (0 mg/kg; placebo). After 60 min of ingestion of the beverages, the swimmers performed a countermovement jump, a maximal handgrip test, a 50 m simulated competition and a 45 s swim at maximal intensity in a swim ergometer. A blood sample was withdrawn 1 min after the completion of the ergometer test. In comparison with the placebo drink, the intake of the caffeinated energy drink increased the height in the countermovement jump (49·4 (sd 5·3) v. 50·9 (sd 5·2) cm, respectively; P<0·05) and maximal force during the handgrip test with the right hand (481 (sd 49) v. 498 (sd 43) N; P<0·05). Furthermore, the caffeinated energy drink reduced the time needed to complete the 50 m simulated swimming competition (27·8 (sd 3·4) v. 27·5 (sd 3·2) s; P<0·05), and it increased peak power (273 (sd 55) v. 303 (sd 49) W; P<0·05) and blood lactate concentration (11·0 (sd 2·0) v. 11·7 (sd 2·1) mm; P<0·05) during the ergometer test. The caffeinated energy drink did not modify the prevalence of insomnia (7 v. 7 %), muscle pain (36 v. 36 %) or headache (0 v. 7 %) during the hours following its ingestion (P>0·05). A caffeinated energy drink increased some aspects of swimming performance in competitive sprinters, whereas the side effects derived from the intake of this beverage were marginal at this dosage.

Epidemiological studies have reported inverse associations between various single healthy diet indices and lower levels of systemic inflammation, but rarely are they examined in the same sample. The aim of the present study was to investigate the potential relationships between biomarkers of systemic inflammation (C-reactive protein (CRP) and fibrinogen) and overall foods (dietary patterns), single foods (fruits and vegetables), and specific nutritive (antioxidants) and non-nutritive (flavonoids) food components in the same narrow-age cohort of older adults. The dietary intake of 792 participants aged 70 years from the Lothian Birth Cohort 1936 was assessed using a 168-item FFQ. Models were adjusted for age, sex, childhood cognitive ability, lifestyle factors and history of disease. Using logistic regression analyses, CRP (normal v. elevated) was favourably associated (at P< 0·05) with the ‘health-aware’ (low-fat) dietary pattern (unstandardised β = (0·200, OR 0·82, 95 % CI 0·68, 0·99) and fruit intake (unstandardised β = (0·100, OR 0·91, 95 % CI 0·82, 0·99), including flavonoid-rich apples (unstandardised β = (0·456, OR 0·63, 95 % CI 0·439, 0·946). Using linear regression analyses, fibrinogen (continuous) was inversely associated (at P< 0·05) with the Mediterranean dietary pattern (standardised β = (0·100), fruit intake (standardised β = (0·083), and combined fruit and vegetable intake (standardised β = (0·084). We observed no association between food components (antioxidant nutrients or specific flavonoid subclasses) and inflammatory markers. In the present cross-sectional study, nutrient-dense dietary patterns were associated with lower levels of systemic inflammation in older people. The results are consistent with dietary guidelines that promote a balanced diet based on a variety of plant-based foods.

Choline is an important nutrient for humans. Choline intake of the European population was assessed considering the European Food Safety Authority European Comprehensive Food Consumption Database and the United States Department of Agriculture Nutrient Database. Average choline intake ranges were 151–210 mg/d among toddlers (1 to ≤3 years old), 177–304 mg/d among other children (3 to ≤10 years old), 244–373 mg/d among adolescents (10 to ≤18 years old), 291–468 mg/d among adults (18 to ≤65 years old), 284–450 mg/d among elderly people (65 to ≤75 years old) and 269–444 mg/d among very elderly people (≥75 years old). The intakes were higher among males compared with females, mainly due to larger quantities of food consumed per day. In most of the population groups considered, the average choline intake was below the adequate intake (AI) set by the Institute of Medicine in the USA. The main food groups contributing to choline intake were meat, milk, grain, egg and their derived products, composite dishes and fish. The main limitations of this study are related to the absence of choline composition data of foods consumed by the European population and the subsequent assumption made to assess their intake levels. Given the definition of AI, no conclusion on the adequacy of choline intake can be drawn for most European population groups. Such results improve the knowledge on choline intake in Europe that could be further refined by the collection of choline composition data for foods as consumed in Europe.

Fe and n-3 long-chain PUFA (n-3 LCPUFA) have both been associated with cognition, but evidence remains inconclusive in well-nourished school-aged children. In the Optimal Well-Being, Development and Health for Danish Children through a Healthy New Nordic Diet (OPUS) School Meal Study, the 3-month intervention increased reading performance, inattention, impulsivity and dietary intake of fish and Fe. This study investigated whether the intervention influenced n-3 LCPUFA and Fe status and, if so, explored how these changes correlated with the changes in cognitive performance. The study was a cluster-randomised cross-over trial comparing school meals with packed lunch (control). At baseline and after each treatment, we measured serum ferritin, whole-blood n-3 LCPUFA and Hb, and performance in reading, mathematics and d2-test of attention. Data were analysed using mixed models (n 726) and principal component analysis of test performances (n 644), which showed two main patterns: ‘school performance’ and ‘reading comprehension’. The latter indicated that children with good reading comprehension were also more inattentive and impulsive (i.e. higher d2-test error%). The intervention improved ‘school performance’ (P=0·015), ‘reading comprehension’ (P=0·043) and EPA+DHA status 0·21 (95 % CI 0·15, 0·27) w/w % (P<0·001), but it did not affect serum ferritin or Hb. At baseline, having small Fe stores was associated with poorer ‘school performance’ in girls, but with better ‘reading comprehension’ in both boys and girls. Both baseline EPA+DHA status and the intervention-induced increase in EPA+DHA status was positively associated with ‘school performance’, suggesting that n-3 LCPUFA could potentially explain approximately 20 % of the intervention effect. These exploratory associations indicate that increased fish intake might explain some of the increase in reading performance and inattention in the study.

Phyto-oestrogens are a family of plant-derived xeno-oestrogens that appear to have beneficial effects on human health. To date, no data are available about phyto-oestrogen consumption affecting liver health in a population. The present study aimed to explore the relationship of urinary phyto-oestrogen metabolites with serum liver enzymes in US adults. A nationally representative sample of US adults in the National Health and Nutrition Examination Survey (NHANES) 2003–10 was analysed. The cross-sectional study sample consisted of 6438 adults with data on urinary phyto-oestrogen levels, serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and γ-glutamyl transaminase (GGT) concentrations and data on other potential confounders. Multivariate logistic regression and linear regression were applied to assess associations between urinary phyto-oestrogen levels and ALT, AST, ALP and GGT concentrations. We found a remarkable association between urinary enterolactone and GGT in both adult males (OR 0·37, 95 % CI 0·22, 0·61; P= 0·003) and females (OR 0·37, 95 % CI 0·26, 0·54; P= 0·009). Moreover, elevated enterolactone levels were inversely associated with ALT and AST levels in adult males. However, no association was present between levels of urinary daidzein, O-desmethylangolensin, equol, enterodiol or genistein with liver enzyme levels in this population. The present study results provide epidemiological evidence that urinary enterolactone levels are associated with liver GGT levels in humans. This suggests a potential protective effect of enterolactone on human liver function. However, the underlying mechanisms still need further investigation.

The SEARCH Nutrition Ancillary Study aims to investigate the role of dietary intake on the development of long-term complications of type 1 diabetes in youth, and capitalise on measurement error (ME) adjustment methodology. Using the National Cancer Institute (NCI) method for episodically consumed foods, we evaluated the relationship between sugar-sweetened beverage (SSB) intake and cardiovascular risk factor profile, with the application of ME adjustment methodology. The calibration sample included 166 youth with two FFQ and three 24 h dietary recall data within 1 month. The full sample included 2286 youth with type 1 diabetes. SSB intake was significantly associated with higher TAG, total and LDL-cholesterol concentrations, after adjusting for energy, age, diabetes duration, race/ethnicity, sex and education. The estimated effect size was larger (model coefficients increased approximately 3-fold) after the application of the NCI method than without adjustment for ME. Compared with individuals consuming one serving of SSB every 2 weeks, those who consumed one serving of SSB every 2 d had 3·7 mg/dl (0·04 mmol/l) higher TAG concentrations and 4·0 mg/dl (0·10 mmol/l) higher total cholesterol and LDL-cholesterol concentrations, after adjusting for ME and covariates. SSB intake was not associated with measures of adiposity and blood pressure. Our findings suggest that SSB intake is significantly related to increased lipid levels in youth with type 1 diabetes, and that estimates of the effect size of SSB on lipid levels are severely attenuated in the presence of ME. Future studies in youth with diabetes should consider a design that will allow for the adjustment for ME when studying the influence of diet on health status.

Modulating the gut microbiota via dietary interventions is a common strategy to enhance the natural defence mechanisms of the host. Several in vitro studies have highlighted the probiotic potential of Bifidobacterium thermophilum RBL67 (RBL67) selected for its anti-Salmonella effects. The present study aimed to investigate the impact of RBL67 alone and combined with fructo-oligosaccharides (FOS) on the gut microbiota of Göttingen minipigs. Minipigs were fed a basal diet supplemented with 8 g/d probiotic powder (1×109 CFU/g in skim milk matrix) (probiotic diet (PRO)), 8 g/d probiotic powder plus 8 g/d FOS (synbiotic diet (SYN)) or 8 g/d skim milk powder (control), following a cross-sectional study design. Faecal and caecal microbiota compositions were analysed with pyrosequencing of 16S rRNA genes and quantitative PCR. Metabolic activity in the caecum and colon was measured by HPLC. 16S rRNA gene amplicon sequencing revealed that minipig faeces show close similarity to pig microbiota. During the treatments and at the time of killing of animals, RBL67 was consistently detected in faeces, caecum and colon at numbers of 105–106 16S rRNA copies/g content after feeding PRO and SYN diets. At the time of killing of animals, significantly higher Bifidobacterium numbers in the caecum and colon of SYN-fed minipigs were measured compared with PRO. Our data indicate that the Göttingen minipig may be a suitable model for gut microbiota research in pigs. Data from this first in vivo study of RBL67 colonisation suggest that the combination with FOS may represent a valuable symbiotic strategy to increase probiotic bacteria levels and survival in gastrointestinal tracts for feed and food applications.

Orally administered probiotic micro-organisms are able to regulate the exacerbated immune response during the antigenic sensitisation process. The aim of the present study was to evaluate the potential efficacy of probiotic fermented milk (PFM) in preventing or treating allergy in an experimental model, and to investigate its underlying mechanisms. Ovoalbumin (OVA)-sensitised BALB/c mice were fed with PFM before the sensitisation procedure or fed continuously with PFM. At 7 and 15 d post-sensitisation, anti-OVA-specific IgE, IgG, IgG1 and IgG2a concentrations were measured in the serum and broncho-alveolar lavage fluid (BALF). Concentrations of interferon-γ (IFN-γ), IL-4, IL-10 and total secretory IgA (S-IgA) were measured in the supernatants of macerated lungs or in the BALF. The levels of IgA+, CD4+ and CD8+ T lymphocytes and F4/80+ cells were measured in the lungs by immunofluorescence. Inducible CD4+/CD25/Foxp3+ regulatory T (Treg) cells were evaluated in the lungs. PFM shifted the T helper (Th)2 profile response towards a Th1 response that led to the production of IgG instead of IgE, with increasing levels of IL-10 and IFN-γ that play an important role in immunomodulation exerted by PFM administration in sensitised mice. Anti-OVA-specific IgE levels were significantly decreased; however, there was no modification in the levels of anti-OVA-specific IgG and total S-IgA. PFM did not influence Treg cells in treated mice. Consumption of PFM could be a promising strategy in the amelioration of airway allergies, considering that the effect is mediated by the production of IgG through the activation of Th1 instead of the direct activation of Th2 cells to produce IgE.

The objective of this study was to examine whether high serum 25-hydroxyvitamin D (25(OH)D) concentration was associated with high skeletal muscle mass, taking into account the effects of sex and age among the participants of the Korea National Health and Nutrition Examination Survey (KNHANES) aged 40 years or older. This was a cross-sectional study using data from the 2009 to 2010 KNHANES; a total of 8406 subjects (3671 men and 4735 women) were included. The appendicular skeletal muscle mass index (ASMMI, kg/m2) was estimated to measure the skeletal muscle mass. Hypovitaminosis was classified when the level of serum 25(OH)D was <20 ng/ml. The general linear model adjusted for confounding factors was used to determine differences in means of ASMMI by 25(OH)D status. The mean values of ASMMI were higher for men when compared with women. Women had a greater proportion of hypovitaminosis (71·1 %) compared with men (53·2 %). After adjusting for multiple factors, men were seen to have significant differences in ASMMI based on 25(OH)D status regardless of age, showing a lower mean value of ASSMI in those with hypovitaminosis. However, there was no difference in ASMMI by 25(OH)D status among women in both younger and older age groups. In conclusion, we found that there might be a positive relationship between 25(OH)D and skeletal muscle mass in men, indicating that interventions to improve 25(OH)D levels that are aimed at increasing muscle mass could be beneficial for men with more rapid decreased rate of skeletal muscle mass.

A higher fat content in the diet could be an advantage for preventing malnutrition among older adults. However, there is sparse scientific evidence to determine the optimal fat intake among older adults. This prospective cohort study examined whether a high energy intake of dietary fat among middle-aged and older adults is associated with the risk of malnutrition 10 years later. The study population comprised 725 Swedish men and women aged 53–80 years who had completed a questionnaire about dietary intake and lifestyle factors in 1997 (baseline) and whose nutritional status was assessed when admitted to the hospital in 2008–2009 (follow-up). At the follow-up, 383 (52·8 %) participants were identified as being at risk of malnutrition and fifty-two (7·2 %) were identified as malnourished. Multinomial logistic regression models were used to analyse the association between previous dietary fat intake and nutritional status later in life. Contrary to what was expected, a high energy intake from total fat, saturated fat and monounsaturated fat among middle-aged and older adults increased the risk of exhibiting malnutrition 10 years later. However, this applied only to individuals with a BMI<25 kg/m2 at the baseline. In conclusion, these findings suggest that preventive actions to counteract malnutrition in older adults should focus on limiting the intake of total fat in the diet by reducing consumption of food with a high content of saturated and monounsaturated fat.