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.

There is a general lack of knowledge regarding the absorption and tissue storage of the provitamin A carotenoid β-cryptoxanthin. The present study investigated the whole-body tissue distribution of β-cryptoxanthin in an appropriate small animal model, the Mongolian gerbil (Meriones unguiculatus), for human provitamin A carotenoid metabolism. After 5 d of carotenoid depletion, five gerbils were euthanised for baseline measurements. The remaining gerbils were placed in three weight-matched treatment groups (n 8). All the groups received 20 μg/d of β-cryptoxanthin from tangerine concentrate, while the second and third groups received an additional 20 and 40 μg/d of pure β-cryptoxanthin (CX40 and CX60), respectively, for 21 d. During the last 2 d of the study, urine and faecal samples of two gerbils from each treatment group were collected. β-Cryptoxanthin was detected in the whole blood, and in twelve of the fourteen tissues analysed. Most tissues resembled the liver, in which the concentrations of β-cryptoxanthin were significantly higher in the CX60 (17·8 (sem 0·7) μg/organ; P= 0·004) and CX40 (16·2 (sem 0·9) μg/organ; P= 0·006) groups than in the CX20 group (13·3 (sem 0·4) μg/organ). However, in intestinal tissues, the concentrations of β-cryptoxanthin increased only in the CX60 group. Despite elevated vitamin A concentrations in tissues at baseline due to pre-study diets containing high levels of vitamin A, β-cryptoxanthin maintained those vitamin A stores. These results indicate that β-cryptoxanthin is stored in many tissues, potentially suggesting that its functions are widespread.

Different regimens of food restriction have been associated with protection against obesity, diabetes and CVD. In the present study, we hypothesised that food restriction would bring benefits to atherosclerosis- and diabetes-prone hypercholesterolaemic LDL-receptor knockout mice. For this purpose, 2-month-old mice were submitted to an intermittent fasting (IF) regimen (fasting every other day) over a 3-month period, which resulted in an overall 20 % reduction in food intake. Contrary to our expectation, epididymal and carcass fat depots and adipocyte size were significantly enlarged by 15, 72 and 68 %, respectively, in the IF mice compared with the ad libitum-fed mice. Accordingly, plasma levels of leptin were 50 % higher in the IF mice than in the ad libitum-fed mice. In addition, the IF mice showed increased plasma levels of total cholesterol (37 %), VLDL-cholesterol (195 %) and LDL-cholesterol (50 %). As expected, in wild-type mice, the IF regimen decreased plasma cholesterol levels and epididymal fat mass. Glucose homeostasis was also disturbed by the IF regimen in LDL-receptor knockout mice. Elevated levels of glycaemia (40 %), insulinaemia (50 %), glucose intolerance and insulin resistance were observed in the IF mice. Systemic inflammatory markers, TNF-α and C-reactive protein, were significantly increased and spontaneous atherosclerosis development were markedly increased (3-fold) in the IF mice. In conclusion, the IF regimen induced obesity and diabetes and worsened the development of spontaneous atherosclerosis in LDL-receptor knockout mice. Although being efficient in a wild-type background, this type of food restriction is not beneficial in the context of genetic hypercholesterolaemia.

Approximately 50 % of patients with inflammatory bowel disease (IBD) suffer from anaemia, with Fe deficiency being the most common cause. CD52 monoclonal antibody (mAb) targets the cell surface CD52 and is effective in depleting lymphocytes through cytolytic effects in vivo. The aim of the present study was to investigate the therapeutic effect of anti-mouse CD52 mAb on Fe-deficient anaemia in IBD. IL-10 knockout mice (IL-10− / −) of 12 weeks with established colitis were treated with anti-mouse CD52 mAb once per week for 2 weeks. Severity of colitis, blood T lymphocytes, blood Hb, haematocrit, plasma erythropoietin (EPO), serum Fe concentration, transferrin saturation, splenic Fe stores, expression of liver hepcidin mRNA, Western blotting of the phosphorylated form of Smad1/5/8 and total Smad1 were measured at the end of the experiment. IL-10− / − mice treated with CD52 mAb showed a reduction in the percentage of CD4+ and CD4+CD45+ T cells in blood and weight loss typically associated with colonic inflammation, serum levels of EPO, the expression of liver hepcidin mRNA and total Smad1 protein, while they showed an increase in Hb concentrations, haematocrit, levels of serum Fe, transferrin saturation and splenic Fe stores. The present results indicated that anti-CD52 therapy may ameliorate Fe-deficient anaemia by reducing colonic inflammation. These findings may open novel horizons in the treatment of patients with IBD by resetting of immunological homeostasis in the gut by depleting the activated T cells in the gut mucosa.

Dietary fish oil modifies skeletal muscle membrane fatty acid composition and oxygen efficiency similar to changes in the myocardium. Oxygen efficiency is a key determinant of sustained force in mammalian skeletal muscle. Therefore, in the present study, we tested the effects of a fish-oil diet on skeletal muscle fatigue under the stress of contraction using the rat in vivo autologous perfused hindlimb model. For 8 weeks, male Wistar rats were fed a diet rich in saturated fat (SF), a diet rich in n-6 PUFA or a diet rich in long-chain (LC) n-3 PUFA DHA derived from fish oil. In anaesthetised, mechanically ventilated rats, with their hindlimbs perfused with arterial blood at a constant flow, the gastrocnemius–plantaris–soleus muscle bundle was stimulated via sciatic nerve (2 Hz, 6–12 V, 0·05 ms) to contract repetitively for 30 min. Rats fed the n-3 PUFA diet developed higher maximum twitch tension than those fed the SF and n-6 PUFA diets (P< 0·05) and sustained twitch tension through more repetitions before the tension declined to 50 % of the maximum twitch tension (P< 0·05). The n-3 PUFA group used less oxygen for tension developed and produced higher venous lactate concentrations with no difference in glycogen utilisation compared with the SF and n-6 PUFA groups. These results further support that incorporation of DHA into skeletal muscle membranes increases the efficiency of oxygen use over a range of contractile force and this is expressed as a higher sustained force and prolonged time to fatigue.

In the existing compartmental models of human vitamin A metabolism, parameters related to the absorption of the isotopic oral dose have not been well identified. We hypothesised that fixing some poorly identified parameters related to vitamin A absorption would improve parameter identifiability and add statistical certainty to such models. In the present study, data for serum vitamin A kinetics in nine subjects given [2H8]retinyl acetate orally and a model with absorption fixed at 75 % were used to test this hypothesis. In addition to absorption efficiency, we fixed two other fractional transfer coefficients: one representing the initial processing of the ingested dose and the other representing the direct secretion of retinol bound to retinol-binding protein (RBP) from enterocytes into the plasma. The Windows version of Simulation, Analysis and Modeling software (WinSAAM) was used to fit serum tracer data v. time for each subject. Then, a population model was generated by WinSAAM's Extended Multiple Studies Analysis. All the parameters had fractional standard deviations < 0·5, and none of the pairs of parameters had a correlation coefficient >0·8 (accepted criteria for well-identified parameters). Similar to the values predicted by the original model, total traced mass for retinol was 1160 (sd 468) μmol, and the time for retinol to appear in the plasma bound to RBP was 31·3 (sd 4·4) h. In conclusion, we suggest that this approach holds promise for advancing compartmental modelling of vitamin A kinetics in humans when the dose must be administered orally.

In the present study, the effect of flax hulls with or without flax oil bypassing the rumen on the expression of lipogenic genes in the mammary tissue of dairy cows was investigated. A total of eight dairy cows were used in a replicated 4 × 4 Latin square design. There were four periods of 21 d each and four treatments: control diet with no flax hulls (CONT); diet with 9·88 % flax hulls in the DM (HULL); control diet with 500 g flax oil/d infused in the abomasum (COFO); diet with 9·88 % flax hulls in the DM and 500 g flax oil/d infused in the abomasum (HUFO). A higher mRNA abundance of sterol regulatory element binding transcription factor, fatty acid (FA) synthase, lipoprotein lipase (LPL), PPARγ1, stearoyl-CoA desaturase (SCD) and acetyl-coenzyme A carboxylase-α was observed in cows fed HULL than in those fed CONT, and HUFO had the opposite effect. Compared with CONT, COFO and HUFO lowered the mRNA abundance of SCD, which may explain the lower proportions of MUFA in milk fat with flax oil infusion. The mRNA abundance of LPL in mammary tissue and proportions of long-chain FA in milk fat were higher in cows fed COFO than in those fed CONT. The highest proportions of trans FA were observed when cows were fed HULL. The present study demonstrates that flax hulls with or without flax oil infusion in the abomasum can affect the expression of lipogenic genes in the mammary tissue of dairy cows, which may contribute to the improvement of milk FA profile.

Gestational methyl donor deficiency (MDD) leads to growth retardation as well as to cognitive and motor disorders in 21-d-old rat pups. These disorders are related to impaired neurogenesis in the cerebral neurogenic areas. Olfactory bulbs (OB), the main target of neuronal progenitors originating from the subventricular zone, play a critical role during the postnatal period by allowing the pups to identify maternal odour. We hypothesised that growth retardation could result from impaired suckling due to impaired olfactory discrimination through imbalanced apoptosis/neurogenesis in the OB. Since neurosteroidogenesis modulates neurogenesis in OB, in the present study, we investigated whether altered neurosteroidogenesis could explain some these effects. Pups born to dams fed a normal diet (n 24) and a MDD diet (n 27) were subjected to olfactory tests during the lactation and weaning periods (n 24 and 20, respectively). We studied the markers of apoptosis/neurogenesis and the expression levels of the key neurosteroidogenic enzyme aromatase, the cholesterol-transfer protein StAR (steroidogenic acute regulatory protein) and the ERα oestrogen receptor and the content of oestradiol in OB. The 21-d-old MDD female pups displayed lower body weight and impaired olfactory discrimination when compared with the control pups. MDD led to greater homocysteine accumulation and more pronounced apoptosis, along with impaired cell proliferation in the OB of female pups. The expression levels of aromatase, StAR and ERα as well as the content of oestradiol were lower in the OB of the MDD female pups than in those of the control female pups. In conclusion, gestational MDD may alter olfactory discrimination performances by affecting neurogenesis, apoptosis and neurosteroidogenesis in OB in a sex-dependent manner. It may be involved in growth retardation through impaired suckling.

The present study investigated the effect of glutamine (Gln) on dextran sulphate sodium (DSS)-induced changes in the expression of small-intestinal intraepithelial lymphocyte (IEL) γδ-T cells in mice. Mice were randomly assigned to a normal control (NC) group and two DSS-treated groups. The NC group and one of the DSS-treated groups (DSS-C) were fed a common semi-purified diet, while the other DSS-treated group (DSS-G) was fed an identical diet, except that part of casein was replaced by Gln, which provided 25 % of total amino acid nitrogen. After being fed the diets for 10 d, mice in the NC group were given distilled water, while the DSS-treated groups were given distilled water containing 2·5 % DSS for 5 d. At the end of the experiment, the mice were killed. The small-intestinal IEL γδ-T-cell subset was isolated for further analysis. The results indicated that DSS treatment resulted in a lower percentage of small-intestinal IEL γδ-T cells and higher mRNA expressions of interferon-γ, TNF-α, IL-17, complement 5a receptor and keratinocyte growth factor in IEL γδ-T cells. Gln administration increased the proportion of small-intestinal IEL γδ-T cells, and the expression levels of immunomodulatory mediator genes in IEL γδ-T cells were lower in the DSS-treated mice. The histological findings indicated that the immunoreactive intensity of the tight junction protein ZO-1 in the small-intestinal mucosa was higher in the DSS-G group than in the DSS-C group. These results indicate that pretreatment with Gln increases the proportion of small-intestinal IEL γδ-T cells and down-regulates γδ-T-cell-expressed inflammatory mediators, which may consequently ameliorate the severity of DSS-induced small-intestinal epithelial injury.

Protein fermentation end products may damage the colonic mucosa, which could be counteracted by dietary inclusion of fermentable carbohydrates (fCHO). Although fermentable crude protein (fCP) and fCHO are known to affect microbial ecology, their interactive effects on epithelial barrier function are unknown. In the present study, in a 2 × 2 factorial experiment, thirty-two weaned piglets were fed low-fCP/low-fCHO (14·5 % crude protein (CP)/14·5 % total dietary fibre (TDF)), low-fCP/high-fCHO (14·8 % CP/16·6 % TDF), high-fCP/low-fCHO (19·8 % CP/14·5 % TDF) and high-fCP/high-fCHO (20·1 % CP/18·0 % TDF) diets. After 21–23 d, samples of proximal and distal colonic mucosae were investigated in Ussing chambers with respect to the paracellular and transcytotic passages of macromolecules and epithelial ion transport. The high-fCHO diets were found to reduce the permeability of the distal colon to the transcytotic marker horseradish peroxidase (HRP, 44 kDa; P <0·05) and also reduce the paracellular permeation of N-hydroxysuccinimide-biotin into the submucosa (443 Da; P <0·05), whereas that of HRP was decreased by the high-fCP diets (P <0·01). Short-circuit current (active ion transport), transepithelial resistance (barrier function) and charge selectivity were largely unaffected in both the segments. However, the high-fCP diets were found to suppress the aldosterone-induced epithelial Na channel activity (P <0·01) irrespective of fCHO inclusion. The high-fCP diets generally reduced the expression of colonic claudin-1, claudin-2 and claudin-3 (P <0·01), while that of claudin-4 was increased by the high-fCHO diets (P <0·01). The high-fCHO diets also altered the ratio between occludin forms (P <0·05) and increased the expression of tricellulin in the proximal colon, which was not observed with high-fCP diets. In conclusion, dietary fCHO and fCP exerted few and largely independent effects on functional measurements, but altered tight junction protein composition in a compensatory way, so that colonic transport and barrier properties were only marginally affected.

Infant microbiota is influenced by numerous factors, such as delivery mode, environment, prematurity and diet (breast milk or formula). In addition to its nutritional value, breast milk contains bioactive substances that drive microbial colonisation and support immune system development, which are usually not present in infant formulas. Among these substances, polyamines have been described to be essential for intestinal and immune functions in newborns. However, their effect on the establishment of microbiota remains unclear. Therefore, the aim of the present study was to ascertain whether an infant formula supplemented with polyamines has an impact on microbial colonisation by modifying it to resemble that in breast-fed neonatal BALB/c mice. In a 4 d intervention, a total of sixty pups (14 d old) were randomly assigned to the following groups: (1) breast-fed group; (2) non-enriched infant formula-fed group; (3) three different groups fed an infant formula enriched with increasing concentrations of polyamines (mixture of putrescine, spermidine and spermine), following the proportions found in human milk. Microbial composition in the contents of the oral cavity, stomach and small and large intestines was analysed by quantitative PCR targeted at fourteen bacterial genera and species. Significantly different (P< 0·05) microbial colonisation patterns were observed in the entire gastrointestinal tract of the breast-fed and formula-fed mice. In addition, our findings demonstrate that supplementation of polyamines regulates the amounts of total bacteria, Akkermansia muciniphila, Lactobacillus, Bifidobacterium, Bacteroides–Prevotella and Clostridium groups to levels found in the breast-fed group. Such an effect requires further investigation in human infants, as supplementation of an infant formula with polyamines might contribute to healthy gastrointestinal tract development.

Mechanisms responsible for derangements in Fe homeostasis in chronic inflammatory conditions are not entirely clear. The aim of the present study was to test the hypothesis that inflammation affects the expression of Fe-related proteins in the duodenum and monocytes of patients with chronic inflammatory disorders, thus contributing to dysregulated Fe homeostasis. Duodenal mucosal samples and peripheral blood monocytes obtained from patients with chronic inflammatory disorders, namely ulcerative colitis (UC), Crohn's disease (CD) and rheumatoid arthritis, were used for gene and protein expression studies. Hb levels were significantly lower and serum C-reactive protein levels were significantly higher in patients in the disease groups. The gene expression of several Fe-related proteins in the duodenum was significantly up-regulated in patients with UC and CD. In patients with UC, the protein expression of divalent metal transporter 1 and ferroportin, which are involved in the absorption of dietary non-haem Fe, was also found to be significantly higher in the duodenal mucosa. The gene expression of the duodenal proteins of interest correlated positively with one another and negatively with Hb. In patients with UC, the gene expression of Fe-related proteins in monocytes was found to be unaffected. In a separate group of patients with UC, serum hepcidin levels were found to be significantly lower than those in the control group. In conclusion, the expression of Fe-related proteins was up-regulated in the duodenum of patients with chronic inflammatory conditions in the present study. The effects appeared to be secondary to anaemia and the consequent erythropoietic drive.

The aim of the present study was to evaluate the impact of infant breast-feeding on cardiovascular risk in young adults. This unique study group involved 158 subjects (eighty-two females) originally collected prospectively at birth in 1975 and followed up to the age of 32 years. Frequent visits during the first year guaranteed the knowledge of the precise duration of breast-feeding. All infants received at least some breast milk. Participants were assessed for both individual cardiovascular risk factors (blood pressure, plasma lipids, homeostatic model assessment of insulin resistance and waist circumference) and the general clinical risk of cardiovascular events by calculating the Framingham risk score (FRS) and the metabolic syndrome criteria score (NCEP-ATPIII; National Cholesterol Education Program's Adult Treatment Panel III). Data on lifestyle factors were carefully collected. Linear regression analyses revealed that the effect of the duration of breast-feeding was not relevant (0·02 decrease in the FRS per one additional breast-feeding month; 95 % CI − 0·19, 0·09). Similarly, the effect of breast-feeding was minor on all of the individual cardiovascular risk factors. We used sex, physical activity, dietary fat and vitamin C, smoking and alcohol consumption as covariates. Again, logistic regression analyses detected no significant impact of the duration of breast-feeding on the risk of the metabolic syndrome according to the NCEP-ATPIII (OR 0·95, 95 % CI 0·8, 1·1). The strongest independent predictor for later CVD risk was male sex. In conclusion, in this prospectively followed cohort of young adults born at term and at weight appropriate for gestational age, the duration of breast-feeding did not have an impact on the accumulation of cardiovascular risk factors.

Fruit and vegetables are key elements of a cardioprotective diet, but benefits on plasma lipids, especially HDL-cholesterol (HDL-C), are inconsistent both within and between studies. In the present study, we investigated whether four selected HDL-C-related polymorphisms (cholesteryl ester transfer protein (CETP) Taq1B, APOA1 − 75G/A, hepatic lipase (LIPC) − 514C → T, and endothelial lipase (LIPG) I24582) modulate the plasma lipid response to a kiwifruit intervention. This is a retrospective analysis of data collected during a 12-week randomised controlled cross-over trial. A total of eighty-five hypercholesterolaemic men completed a 4-week healthy diet run-in period before being randomised to one of two 4-week intervention sequences of two green kiwifruit/d plus healthy diet (kiwifruit intervention) or healthy diet alone (control intervention). The measurement of anthropometric parameters and collection of fasting blood samples were carried out at baseline 1 and after the run-in (baseline 2) and intervention periods. At baseline 2, B1/B1 homozygotes of the CETPTaq1B gene had significantly higher total cholesterol:HDL-C, TAG:HDL-C, and apoB:apoA1 ratios and small-dense LDL concentrations than B2 carriers. A significant CETP Taq1B genotype × intervention interaction was observed for the TAG:HDL-C ratio (P= 0·03). B1/B1 homozygotes had a significantly lower TAG:HDL-C ( − 0·23 (sd 0·58) mmol/l; P= 0·03) ratio after the kiwifruit intervention than after the control intervention, whereas the ratio of B2 carriers was not affected. The lipid response was not affected by other gene polymorphisms. In conclusion, the significant decrease in the TAG:HDL-C ratio in B1/B1 homozygotes suggests that regular inclusion of green kiwifruit as part of a healthy diet may improve the lipid profiles of hypercholesterolaemic men with this genotype.

A combination of high folate with low vitamin B12 plasma status has been associated with cognitive impairment in a population exposed to mandatory folic acid fortification. The objective of the present study was to examine the interactions between plasma concentrations of folate and vitamin B12 markers in relation to cognitive performance in Norwegian elderly who were unexposed to mandatory or voluntary folic acid fortification. Cognitive performance was assessed by six cognitive tests in 2203 individuals aged 72–74 years. A combined score was calculated using principal component analysis. The associations of folate concentrations, vitamin B12 markers (total vitamin B12, holotranscobalamin (holoTC) and methylmalonic acid (MMA)) and their interactions in relation to cognitive performance were evaluated by quantile regression and least-squares regression, adjusted for sex, education, apo-ɛ4 genotype, history of CVD/hypertension and creatinine. Cross-sectional analyses revealed an interaction (P= 0·009) between plasma concentrations of folate and vitamin B12 in relation to cognitive performance. Plasma vitamin B12 concentrations in the lowest quartile ( < 274 pmol/l) combined with plasma folate concentrations in the highest quartile (>18·5 nmol/l) were associated with a reduced risk of cognitive impairment compared with plasma concentrations in the middle quartiles of both vitamins (OR 0·22, 95 % CI 0·05, 0·92). The interaction between folate and holoTC or MMA in relation to cognitive performance was not significant. In conclusion, this large study population unexposed to mandatory folic acid fortification showed that plasma folate, but not plasma vitamin B12, was associated with cognitive performance. Among the elderly participants with vitamin B12 concentrations in the lower range, the association between plasma folate and cognitive performance was strongest.

Fat-soluble vitamins A, E and K have been shown to play roles in immunity and inflammation, but studies on child allergic disease have been few and inconsistent. The aim of the present study was to examine the relationship between maternal intake of vitamins A, E and K in mid-pregnancy and child asthma and allergic rhinitis. We used data on 44 594 mother–child pairs from the Danish National Birth Cohort. Maternal intake of fat-soluble vitamins was calculated based on the information from a validated FFQ completed in mid-pregnancy. At 18 months, interviews with the mothers were conducted to evaluate doctor-diagnosed child asthma. At age 7 years, we assessed child asthma and allergic rhinitis using questions from the International Study of Asthma and Allergies in Childhood questionnaire and by national registries on hospital contacts and medication use. Current asthma was defined as asthma diagnosis and wheeze in the past 12 months by maternal report. We calculated multivariable risk ratios and 95 % CI by comparing the highest v. lowest quintile (Q) of maternal vitamin A, E and K intake in relation to child allergic disease outcomes. Maternal total vitamin K intake was directly associated with ever admitted asthma (Q5 v. Q1: 1·23, 95 % CI 1·01, 1·50) and current asthma at 7 years (Q5 v. Q1: 1·30, 95 % CI 0·99, 1·70). Weak inverse associations were present for maternal vitamin A and E intake during pregnancy with child allergic rhinitis. Maternal vitamin K intake during pregnancy may increase the risk of child asthma, and should be explored further on a mechanistic level. Conversely, maternal vitamin A and E intake may protect against child allergic rhinitis.

Several N-nitroso compounds (NOC) have been shown to be carcinogenic in a variety of laboratory animals, but evidence of their carcinogenicity in humans is lacking. We aimed to examine the association between NOC intake and colorectal cancer (CRC) risk and possible effect modification by vitamins C and E and protein in a large case–control study carried out in Newfoundland and Labrador and Ontario, Canada. A total of 1760 case patients with pathologically confirmed adenocarcinoma and 2481 population controls were asked to complete a self-administered FFQ to evaluate their dietary intakes 1 year before diagnosis (for cases) or interview (for controls). Adjusted OR and 95 % CI were calculated across the quintiles of NOC (measured by N-nitrosodimethylamine (NDMA)) intake and relevant food items using unconditional logistic regression. NDMA intake was found to be associated with a higher risk of CRC (highest v. lowest quintiles: OR 1·42, 95 % CI 1·03, 1·96; P for trend = 0·005), specifically for rectal carcinoma (OR 1·61, 95 % CI 1·11, 2·35; P for trend = 0·01). CRC risk also increased with the consumption of NDMA-containing meats when the highest tertile was compared with the lowest tertile (OR 1·47, 95 % CI 1·03, 2·10; P for trend = 0·20). There was evidence of effect modification between dietary vitamin E and NDMA. Individuals with high NDMA and low vitamin E intakes had a significantly increased risk than those with both low NDMA and low vitamin E intakes (OR 3·01, 95 % CI 1·43, 6·51; P for interaction = 0·017). The present results support the hypothesis that NOC intake may be positively associated with CRC risk in humans. Vitamin E, which inhibits nitrosation, could modify the effect of NDMA on CRC risk.

High consumption of refined grains, particularly white rice, has been reported to be associated with a higher risk of type 2 diabetes. Therefore, in the present study, we evaluated the association between rice and noodle consumption and markers of glucose homeostasis, inflammation and dyslipidaemia in an Asian population. We carried out a population-based cross-sectional study in 2728 Singaporean Chinese men and women aged between 24 and 92 years. Rice and noodle intake was assessed using a validated FFQ and studied in relation to glycaemic (fasting glucose, glycated Hb, homeostasis model assessment (HOMA) index for insulin resistance (HOMA-IR) and HOMA index for β-cell function (HOMA-β)), inflammatory (plasma adiponectin and C-reactive protein (CRP)) and lipid (fasting TAG and HDL-cholesterol (HDL-C)) markers. We used multiple linear regression analyses with adjustment for total energy intake and sociodemographic, anthropometric (BMI and waist:hip ratio) and lifestyle factors. Higher rice consumption was found to be associated with higher fasting glucose concentrations (0·81 % higher values per portion increment; 95 % CI 0·09, 1·54) and HOMA-IR (4·62 %; 95 % CI 1·29, 8·07). Higher noodle consumption was also found to be significantly associated with higher fasting glucose concentrations (1·67 %; 95 % CI 0·44, 2·92), HOMA-IR (6·17 %; 95 % CI 0·49, 12·16) and fasting TAG concentrations (9·17 %; 95 % CI 3·44, 15·22). No significant association was observed between rice and noodle consumption and adiponectin, CRP and HDL-C concentrations or HOMA-β in the fully adjusted model. These results suggest that high consumption of rice and noodles may contribute to hyperglycaemia through greater insulin resistance and that this relationship is independent of adiposity and systemic inflammation.

Prevalence rates of malnutrition vary considerably internationally, partly due to differences in measurement methodology and instruments. In the present study, the same measurement methodology and instruments were used in The Netherlands, Germany and Austria. The aim of the present study was to investigate whether resident characteristics influence possible differences in malnutrition prevalence between countries. The study followed a cross-sectional, multi-centre design that measured malnutrition in nursing home residents from The Netherlands, Germany and Austria. Resident data were gathered using a standardised questionnaire. Malnutrition was operationalised using BMI, unintentional weight loss and nutritional intake. Data were analysed using an association model. The prevalence rates of malnutrition in The Netherlands, Germany and Austria were 18·3, 20·1 and 22·5 %, respectively. The multivariate generalised estimating equation (GEE) logistic regression analysis showed that sex, age, care dependency, the mean number of diseases and some specific diseases were influencing factors for whether the resident was malnourished or not. The OR of malnutrition in the three countries declined after including the influencing factors resulting from the multivariate GEE analysis. The present study reveals that differences in the prevalence rates of malnutrition in nursing homes in The Netherlands, Germany and Austria are influenced by different resident characteristics. Since other country-related factors could also play an important role in influencing differences in the prevalence rates of malnutrition between the countries (structural and process factors of malnutrition care policy). We recommend the investigation of these factors in future studies.