Fe absorption is affected by many dietary factors. The objective of the present study was to measure the effects of high v. low content of vitamin C, meat and phytic acid in whole diets with Fe-fortified bread on the efficacy of Fe absorption. Thirty-two healthy women with low Fe stores were randomised to three groups, each of which was given two of six test diets containing either low/high amounts of vitamin C, meat or phytic acid, respectively, in a cross-over design. Each diet was served throughout a 5 d period. Fe-fortified rye bread, extrinsically labelled with 59Fe, was given with all main meals. Fe absorption was determined from whole-body counter measurements of 59Fe retention. The fractional non-haem Fe absorption (corrected to a 40% standard absorption by measurements from the reference dose) was 1·9% v. 3·4% (P=0·04) for the low/high vitamin C diets, 3·0% v. 3·5% (P=0·58) on the low/high meat diets and 4·9% v. 3·8% (P=0·24) on the low/high phytic acid diet, respectively. The total Fe absorbed (geometric mean with standard error) varied from 0·43 (se 0·11) mg from the diet with lowest bioavailability to 1·09 (se 0·18) mg from the diet with highest bioavailability (P<0·001). The present whole-diet study indicates that diet composition is a strong predictor of Fe absorption. In the diet with a low content of enhancers and a high content of inhibitors, vitamin C improved non-haem Fe absorption. The total Fe absorption varied 2·5-fold after small alterations of the content of enhancers and inhibitors in the diet.

Normal odd-chain SFA (OCSFA), particularly tridecanoic acid (n-13 : 0), pentadecanoic acid (n-15 : 0) and heptadecanoic acid (n-17 : 0), are normal components of dairy products, beef and seafood. The ratio of n-15 : 0:n-17 : 0 in ruminant foods (dairy products and beef) is 2:1, while in seafood and human tissues it is 1:2, and their appearance in plasma is often used as a marker for ruminant fat intake. Human elongases encoded by elongation of very long-chain fatty acid (ELOVL)1, ELOVL3, ELOVL6 and ELOVL7 catalyse biosynthesis of the dominant even-chain SFA; however, there are no reports of elongase function on OCSFA. ELOVL transfected MCF7 cells were treated with n-13 : 0, n-15 : 0 or n-17 : 0 (80 µm) and products analysed. ELOVL6 catalysed elongation of n-13 : 0→n-15 : 0 and n-15 : 0→n-17 : 0; and ELOVL7 had modest activity toward n-15 : 0 (n-15 : 0→n-17 : 0). No elongation activity was detected for n-17 : 0→n-19 : 0. Our data expand ELOVL specificity to OCSFA, providing the first molecular evidence demonstrating ELOVL6 as the major elongase acting on OCSFA n-13 : 0 and n-15 : 0 fatty acids. Studies of food intake relying on OCSFA as a biomarker should consider endogenous human metabolism when relying on OCSFA ratios to indicate specific food intake.

Our laboratory has reported that n-3 PUFA can reduce host resistance to Listeria infection, in part, by impairing in vivo IL-12 biosynthesis. Recently, PUFA were shown to be ligands for PPAR, a novel family of nuclear receptors with three isoforms: PPARα, PPARδ/β and PPARγ. PPARγ is expressed in immune cells, such as T cells and macrophages. Two PPARγ agonists, 15-deoxy-Δ12,14-prostaglandin (PG) J2 and rosiglitazone, have been shown to have immunomodulatory activity in vitro, including inhibiting IL-12 biosynthesis. We hypothesized that n-3 PUFA inhibit IL-12 production through activating PPARγ. We used thioglycolate-elicited mouse peritoneal macrophages to study the effect of various fatty acids and their oxidized metabolites on in vitro IL-12 production. Our present results demonstrate that both n-3 and n-6 PUFA can reduce in vitro IL-12 biosynthesis, though less potently than 15-deoxy-PGJ2 and rosiglitazone. GW9662, a PPARγ antagonist, reversed the inhibitory effect of rosiglitazone, but not that of PUFA. Our present findings suggest that fatty acid-mediated inhibition of IL-12 production is independent of PPARγ.

We carried out this study to compare the effect of consuming whole, partially defatted and defatted cows’ milk for 4 months on serum concentrations of blood indicators of cardiovascular risk (CVR) in Mexican children and adolescents. Children aged between 6 and 16 years living in indigenous boarding schools in Mexico and who were usual consumers of whole milk were recruited to this study. Totally, thirteen boarding schools were randomly selected to receive full supplies of whole, partially defatted and defatted cows’ milk for 4 months. Serum total cholesterol (TC), TAG, HDL-cholesterol, apoA and total apoB, and Lp(a) concentrations were measured before and after the intervention. Comparisons were made with multi-level mixed-effects linear regression models using the difference in differences approach. Compared with the whole milk group, TC, LDL-cholesterol, HDL-cholesterol and total apoB were lower in defatted milk consumers by –0·43, –0·28, –0·16 mmol/l and −0·05 g/l, respectively (all P<0·001). Compared with the whole milk group, the group that consumed partially defatted milk showed a significant decrease in the concentrations of LDL-cholesterol (−0·12, P=0·01), apoA (−0·05 g/l, P=0·01) and total apoB (−0·05 g/l, P=0·001). Defatted milk intake for 4 months reduced some of the serum indicators of CVR.

This experiment aimed to investigate the influence of folic acid supplements on the carry-over of folates from the sow to the fetus during late gestation and to the suckling piglet. Two groups of sixteen German Landrace sows received, during gestation and lactation, a diet supplemented with either 0 or 10 mg folic acid/kg. Increased folic acid concentrations in the serum of sows were detected only at the end of gestation (day 100) and at the end of lactation (day 28). The supplementation with folic acid to the sows' diet improved the folic acid supply of the fetus compared with unsupplemented controls; values were respectively 92.6 v. 56.2 nmol folates/l serum in newborn piglets and 171.9 v. 76.3 μmol folates/g fresh liver in stillborn piglets (P < 0.05). Folate concentrations in colostrum and milk (day 28) were 3.6- and 5.0-times higher in supplemented than unsupplemented sows. This treatment effect was also reflected in the serum of piglets until weaning. Therefore, the folic acid supply for the suckling piglet is dependent mainly upon the carry-over of maternal folates via colostrum and milk.

Dietary patterns describe the combination of foods and beverages in a diet and the frequency of habitual consumption. Better understanding of childhood dietary patterns and antenatal influences could inform intervention strategies to prevent childhood obesity. We derived empirical dietary patterns in 1142 children (average age 6·0 (sd 0·2) years) in New Zealand, whose mothers had participated in the Screening for Pregnancy Endpoints (SCOPE) cohort study and explored associations with measures of body composition. Participants (Children of SCOPE) had their diet assessed by FFQ, and dietary patterns were extracted using factor analysis. Three distinct dietary patterns were identified: ‘Healthy’, ‘Traditional’ and ‘Junk’. Associations between dietary patterns and measures of childhood body composition (waist, hip, arm circumferences, BMI, bioelectrical impedance analysis-derived body fat % and sum of skinfold thicknesses (SST)) were assessed by linear regression, with adjustment for maternal influences. Children who had higher ‘Junk’ dietary pattern scores had 0·24 (sd 0·08; 95 % CI 0·04, 0·13) cm greater arm and 0·44 (sd 0·05; 95 % CI 0·01, 0·10) cm greater hip circumferences and 1·13 (sd 0·07; 95 % CI 0·03, 0·12) cm greater SST and were more likely to be obese (OR 1·74; 95 % CI 1·07, 2·82); those with higher ‘Healthy’ pattern scores were less likely to be obese (OR 0·62; 95 % CI 0·39, 1·00). In a large mother–child cohort, a dietary pattern characterised by high-sugar and -fat foods was associated with greater adiposity and obesity risk in children aged 6 years, while a ‘Healthy’ dietary pattern offered some protection against obesity. Targeting unhealthy dietary patterns could inform public health strategies to reduce the prevalence of childhood obesity.

Practice guidelines for non-alcoholic fatty liver disease (NAFLD) recommend promoting the Mediterranean dietary pattern (MDP) which is cardioprotective and may improve hepatic steatosis. This study aimed to explore multidisciplinary clinicians’ perspectives on whether the MDP is recommended in routine management of NAFLD and barriers and facilitators to its implementation in a multi-ethnic setting. Semi-structured individual interviews were conducted with fourteen clinicians (seven doctors, three nurses, three dietitians and one exercise physiologist) routinely managing patients with NAFLD in metropolitan hospital outpatient clinics in Australia. Interviews were audio-recorded, transcribed and analysed using thematic content analysis. Clinicians described that lifestyle modification was their primary treatment for NAFLD and promoting diet was recognised as everyone’s role, whereby doctors and nurses raise awareness and dietitians provide individualisation. The MDP was regarded as the most evidence-based diet choice currently and was frequently recommended in routine care. Facilitators to MDP implementation in practice were: improvement in diet quality as a parallel goal to weight loss; in-depth knowledge of the dietary pattern; access to patient education and monitoring resources and; service culture, including an interdisciplinary clinic goal, and knowledge sharing from expert dietitians. Barriers included perceived challenges for patients from diverse cultural and socio-economic backgrounds and limited clinician training, time and resourcing to support behaviour change. Integration of MDP in routine management of NAFLD in specialist clinics was facilitated by a focus on diet quality, knowledge sharing, belief in evidence and an interdisciplinary team. Innovations to service delivery could better support and empower patients to change dietary behaviour long-term.

Using the World Health Organization criterion, the prevalence of sub-clinical vitamin A deficiency can be assessed using plasma retinol concentrations <0·7 μmol/l. However, plasma retinol can be depressed by infection; thus, the use of this criterion alone may overestimate deficiency. In the present study, we investigated the usefulness of the acute-phase proteins (APP) α1-antichymotrypsin (ACT) and α1-acid glycoprotein (AGP), plasma carotenoids and anthropometric and gestational indices to interpret plasma retinol in the blood of 192 apparently healthy Nigerian neonates collected randomly during days 1–20 postpartum. The mean weight (2·64 kg) and length (0·458 m) of the neonates and plasma concentrations (geometric mean, μmol/l) of retinol (0·54), α-carotene (0·072), ß-carotene (0·076) and lutein (0·080) were low. The prevalence of vitamin A deficiency was 72 %, indicating a severe public health problem. Babies who were of low birth weight (P<0·003) or premature and low birth weight (P<0·023) had significantly lower retinol concentrations than full-term normal weight babies. Thirty-two neonates had abnormal ACT and forty-four abnormal AGP concentrations. Positive correlations between retinol and ACT (r 0·186, P=0·05) and AGP (r 0·31, P=0·0001) during days 1–5 may be due to the increasing plasma retinol from maternal milk and a coincidental increasing capacity to synthesise APP. Subsequently, negative correlations between retinol and ACT (r −0·28, P=0·02) and AGP (r −0·29, P=0·018) from day 6 onwards reflected the continuing increase in plasma retinol, but no further increase in the APP. Overall, weight, ACT, lutein and age explained 30 % of the variance in retinol, but lutein was the most significant (r2 0·18, P<0·0001). Hence, the distribution of plasma retinol concentrations in this group of neonates was more strongly linked with nutrition (via the surrogate marker lutein) than infection.

Pro-inflammatory cytokines play a key role in many models of hepatic damage. In addition, asparagine (Asn) plays an important role in immune function. We aimed to investigate whether Asn could attenuate lipopolysaccharide (LPS)-induced liver damage. Forty-eight castrated barrows were allotted to four groups including: (1) non-challenged control; (2) LPS-challenged control; (3) LPS+0·5 % Asn; and (4) LPS+1·0 % Asn. After 19 d feeding with control, 0·5 or 1·0 % Asn diets, pigs were injected with LPS or saline. Blood and liver samples were obtained at 4 h (early stage) and 24 h (late stage) post-injection. Asn alleviated liver injury, indicated by reduced serum aspartate aminotransferase and alkaline phosphatase activities linearly and quadratically; it increased claudin-1 protein expression linearly and quadratically at 24 h, and less severe liver morphological impairment at 4 or 24 h. In addition, Asn decreased mRNA expression of TNF-α and heat shock protein 70 (HSP70) linearly and quadratically at 4 h; it increased TNF-α mRNA expression, and HSP70 protein expression linearly and quadratically at 24 h. Moreover, Asn increased inducible NO synthase activity linearly and quadratically. Finally, Asn down-regulated the mRNA expression of Toll-like receptor 4 (TLR4) signalling molecules (TLR4, IL-1 receptor-associated kinase 1 (IRAK1), TNF-α receptor-associated factor 6), nucleotide-binding oligomerisation domain protein (NOD) signalling molecules (NOD1, NOD2 and their adaptor molecule receptor-interacting serine/threonine-protein kinase 2 (RIPK2)), and NF-κB p65 linearly or quadratically at 4 h. Oppositely, Asn up-regulated mRNA expressions of TLR4 and NOD signalling molecules (TLR4, myeloid differentiation factor 88, IRAK1, NOD2 and RIPK2), and their negative regulators (radioprotective 105, single Ig IL-1R-related molecule, Erbb2 interacting protein and centaurin β1) linearly or quadratically at 24 h. These results indicate that, in early and late stages of LPS challenge, Asn improves liver integrity and exerts different regulatory effects on mRNA expression of TLR4 and NOD signalling molecules.

1. A cereal-based diet containing 7.6 mg copper/kg was fed ad lib. to laying hens for up to 48 d. Four other groups were given the control diet to which was added hydrated copper sulphate to provide 250, 500, 1000 and 2000 mg added Cu/kg.

2. Hens were killed on day o and after 3, 6, 12, 24 and 48 d. Records were kept of body-weight, food consumption, egg production and egg weight.

3. After slaughter blood haemoglobin, packed cell volume, serum Cu and aspartate aminotransfferase- (AAT; EC 2.6. I. I) were measured. The liver, kidneys, a sample of breast muscle, oviduct, ovary and gizzard were weighed. Gizzard, spleen. liver and kidney tissue were examined histologically.

4. The Cu, zinc and iron concentrations of liver, kidneys and breast muscle and the manganese concentrations of liver and kidneys were determined.

5. Body-weight loss occurred at 500–2000mg added Cu/kg diet. Egg production was depressed by level of added Cu and period of time on the Cu-containing diets.

6. Mean liver, kidney, oviduct and ovarian weights per unit body-weight were depressed by Cu in the diet and the effect increased with period of time on the diets. Mean gizzard weight per unit body-weight was increased by dietary added Cu and by time.

7. Cu concentrations in the liver were increased by dietary level of added Cu and period of timeon the diet. Zn concentration in liver increased at 1000 and 2000 mg added Cu/kg diet and liver Fe concentration was increased at these levels. Histological examination of the gizzard indicated that the Cu content of the gizzard lining increased with dietary added Cu.

To explore whether the metabolic responses to trans, compared with cis, fatty acids depend on the source of dietary polyunsaturated fatty acids (PUFA), male Sprague-Dawley rats, 5 weeks old, were fed on diets containing 30 g oleic (cis) or elaidic (trans) acids/kg in combination with either 70 g perilla oil (α-linolenic acid) or safflowerseed oil (linoleic acid)/kg for 3 weeks in separate experiments. The dietary fats were adjusted to have the same level of total PUFA. The dietary manipulation did not influence the growth indices, but spleen weight was greater when the dietary PUFA source was perilla oil. The incorporation of trans fatty acid into liver phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol and phosphatidylserine and adipose tissue lipids, particularly phospholipids, was significantly higher when rats were fed on safflowerseed oil compared with perilla oil. However, only limited differences were observed in the effects of cis and trans fatty acids on the proportions of PUFA in liver phospholipids. Splenic production of prostaglandin E2 was reduced by trans fatty acid when safflowerseed oil was the PUFA source, but no trans effect was observed on leukotriene C4 production. Dietary PUFA significantly influenced the concentration of plasma immunoglobulins (Ig) but the effect of geometry was only seen in IgG which was increased by trans acid. Dietary trans fatty acid increased the CD4+: CD8+ T-lymphocyte ratio in the spleen, reflecting a decreasing trend of the proportion of CD8+, when combined with perilla oil. These observations indicate that the type of PUFA simultaneously ingested specifically infiuences the effect that trans acid exerts on PUFA metabolism, eicosanoid production and some immune indices.

1. Plant foods, especially green leafy vegetables, are the cheapest and richest source of calcium in developing countries and are recommended in balanced diets. Hence it was worth while obtaining further information about the availability of Ca from these commonly-consumed green leaves.

2. The green leafy vegetable belonging to Amaranthus spp. was taken as a suitable experimental model because it is not only commonly-consumed, but is also rich in Ca and oxalates. In the first experiment, each of the eight adult male subjects was given a basal diet containing negligible Ca, a milk diet and an ‘Amaranthus’ diet, both containing the same amount of Ca. These diets were given on 3 consecutive days and the urinary Ca excreted in a 6 h period after the test diet was considered an approximate index of Ca absorbed in that period. The second experiment was designed to study the influence of Amaranthus spp. on the availability of milk Ca. Each of the ten adult male subjects were given a basal diet, a milk diet and a diet containing the same amount of milk with Amaranthus spp. added to it. Urinary Ca excreted in a period of 6 h was estimated.

3. While availability of Ca from milk was good, that from Amaranthus leaves was low. The ingestion of Amaranthus leaves together with milk adversely affected the absorption of milk Ca.

4. In view of these findings, recommendation of green leaves as a regular source of Ca to the vulnerable section of the Indian Community should be considered with caution. Since green leaves are a main source of other nutrients, especially β-carotene, their consumption cannot be discouraged and hence leaves low in oxalates should be recommended.

Dietary intake characteristics were studied among 3833 adults of the second Dutch National Food Consumption Survey held in 1992. The subjects were classified into three groups based on their intake of total fat (% energy), saturated fatty acids (% energy), dietary fibre (g/MJ), and fruit and vegetables (g/d). All the classifications resulted in differences in energy intake. Except for dietary fibre, the mean energy intake was higher in the higher-intake tertiles. For the classification based on total fat, saturated fatty acids and dietary fibre the more prudent diets were accompanied with a lower energy-intake. As to the consumption of food groups, differences existed in both the proportion of consumers and in the mean consumption among users. It is concluded that the trends observed are probably more important than the actual figures.

Polycyclic aromatic hydrocarbons (PAH) are procarcinogens that can be commonly found in our food and environment. Upon biotransformation in our body system, they can cause DNA damage through the generation of genotoxic species and oxidative stress. Phase I and II enzymes are pivotal in the process of proximate carcinogen formation and elimination. Some dietary phytochemicals are strong inhibitors to the phase I enzymes. In the present study, we investigated the effect of the red wine compound resveratrol on DNA damage induced by PAH in a non-tumorigenic breast cell line MCF-10A. Resveratrol ranging from 1 to 5 μm could significantly suppress the expressions of cytochrome P450 (CYP) 1A1, CYP1B1 and UDP-glucuronosyltransferase (UGT) 1A1 induced by 7,12-dimethylbenz[a]anthracene (DMBA). The comet assay indicated that DMBA introduced DNA damage to these cells, and co-treatment of resveratrol at 5 or 10 μm could alleviate the damage. Further investigation illustrated that resveratrol reduced the binding of DMBA metabolites to DNA with no effect on DMBA-induced oxidative DNA damage. Since the phase II enzyme UGT1A1 was suppressed, the elimination of DMBA metabolites would not have contributed to the reduction in the DMBA metabolite–DNA binding. In summary, resveratrol might protect breast cells against PAH-induced DNA damage. The underlying mechanism was mediated by phase I enzyme suppression rather than phase II enzyme induction or oxidative DNA repair.