Eight Friesian calves were reared from birth to the start of the experiment at a predetermined growth rate of 1.0 kg/d. Four calves (group 1) commenced the experiment at 22 weeks of age and the remainder (group 2) at 34 weeks, and feed intake was calculated to provide sufficient metabolizable energy to sustain zero energy balance (Em). Between experimental days 30 and 56 at maintenance levels of feeding, respiratory exchange measurements were made using open-circuit calorimetry to provide indirect estimates of heat production (H) simultaneous with measurements of faecal and urinary excretion of energy and N. A datum point for Em and H was established for each animal giving mean values for Em of 491 and 537 and for H of 476 and 511 kJ/kg live weight (LW)0.75 per d for groups 1 and 2 respectively. Treatment levels calculated as 0·25, 0·5, 0·75 and 1·25 of dry matter intake required to sustain the measured Em, were imposed on individual animals after day 56 and further measurements of H and faecal/ urinary balance were made between days 72 and 84 followed by measurements of fasting heat production (FHP) during days 86–90 from the two animals in each group which had received the 0.75 and 1.25 levels of intake. Regression analysis of the treatment levels indicated separate linear models which predicted Em at 419 and 473 kJ/kg LW0·75 per d for groups 1 and 2 respectively. The incorporation of FHP with partitioning of faecal and urinary energy losses measured during fasting altered the relationship but not the predicted Em. Overall predicted Em (days 72–84) from all models were 406 and 478 kJ/kg LW0.75 per d for groups 1 and 2 respectively which were significantly lower (P < 0·05) than Em measured during days 30–56.

1. Q-strain mice selected for high (QLF) or low (QSC) body-weight at 6 weeks of age were compared with respect to their body-weight increases, gross body compositions and food intakes.

2. DNA, RNA, protein and hydroxyproline contents were measured.

3. QLF animals were larger at all stages of development but ate more food and gained more body-weight per unit food intake with an apparently improved efficiency of utilization compared with QSC mice.

4. The efficiency of deposition of dietary energy in Q-strain mice was found to be significantly lower than that of other growing mammals receiving similar energy intakes.

5. Body water, protein and fat of both strains were similar at birth and at 42 d of age but the contribution of fat to body-weight in the preweaning phase was greater for QLF while QSC accreted more fat per unit weight gain in the postweaning period.

6. An increase in cell number made a greater contribution to the growth post partum of the QLF mice, but by 42 d of age little difference between the number of cells per unit weight in the two strains was evident.

7. Despite increases in RNA concentrations at all stages of development, of QLF mice compared with QSC, measurements of body composition do not indicate any accompanying increases of protein concentration in these animals.

This study determined the validity, reproducibility and usability of a smartphone app – APPetite – for the measure of free-living, subjective appetite. Validity was assessed compared with the criterion tool of pen-and-paper visual analogue scale (VAS) (n 22). Appetite was recorded using APPetite and VAS, one immediately after the other, upon waking and every hour thereafter for 12 h. This was repeated the next day with the order of tool reversed. Agreement between tools was assessed using Bland–Altman analysis. Reproducibility and usability were assessed in a separate experiment (n 22) of two trials (APPetite v. VAS), separated by 7 d. Appetite was recorded in duplicate upon waking and every hour for 12 h using APPetite or VAS. Agreement between duplicate measures was assessed using Bland–Altman analysis and CV was compared between tools. Usability was assessed by comparing compliance and by qualitative evaluation. APPetite demonstrated good criterion validity with trivial bias of 1·65 units/mm·h–1 between APPetite- and VAS-derived AUC appetite scores. Limits of agreement were within a maximum allowed difference of 10 %. However, proportional bias was observed. APPetite demonstrated high reproducibility, with minimal bias (–0·578 units·h–1) and no difference in CV between APPetite and VAS (1·29 ± 1·42 % v. 1·54 ± 2·36 %, P = 0·64). Compliance was high with APPetite (92·7 ± 8·0 %) and VAS (91·6 ± 20·4 %, P = 0·81). Ninety percent of participants preferred APPetite, citing greater accessibility, simplified process and easier/quicker use. While proportional bias precludes using APPetite and VAS interchangeably, APPetite appears a valid, reproducible and highly usable tool for measuring free-living appetite in young-to-middle-aged adults.

Excess body weight confers a high risk to human health. Body weight variation between subjects can be partially explained by genetic differences. The aim of the present study was to investigate the association of genetic variants in the ADIPOQ (rs2241766) and LEP (rs7799039) genes with body weight trajectories in children from birth to 6 years of age. This was a prospective cohort (PREDI Study). Socio-economic, biological and anthropometric data were collected at four time points: at birth in the maternity unit; 1–2, 4–5 and 6 years old at the participants’ homes. Genotyping was performed by PCR-restriction fragment length polymorphism. Poisson regression and linear mixed-effect regression models were used to address the association of ADIPOQ and LEP genotypes with BMI. Excessive body weight at pre-pregnancy (β = 0·339, P = 0·01) and excessive gestational weight gain (β = 0·51, P < 0·001) were associated with children’s BMI trajectory from birth to 6 years. The ADIPOQ-rs2241766 TG or GG genotype was associated with a higher risk of excess body weight in the first 6 years of life (both sexes relative risk 1·25, 95 % CI 1·01, 1·56; female relative risk 1·67, 95 % CI 1·20, 2·31). BMI increased over the years according to the presence of the TG or GG genotype (β = 0·01, 95 % CI 0·01, 0·02), particularly in females (β = 0·02, 95 % CI 0·01, 0·04). The ADIPOQ-rs2241766 TG and GG genotypes increased the risk of excess body weight in children from birth to 6 years of age and had a positive effect on body weight trajectories in girls. The LEP-rs7799039 genetic variant was not associated with body weight trajectory in children.

Although the impact of diet on physical health is an important public health issue, less attention has been devoted to the relationship between nutrition and children’s mental development. The views of parents and teachers about the extent to which diet affects physical and mental development of children were compared in four European countries. An online questionnaire (developed in English and translated) was circulated through a market research agency. Participants were parents or teachers of children aged 4–10 years without learning or behavioural issues. Questionnaires were returned by 1606 parents (401 in England, Germany and Hungary; 403 in Spain) and 403 teachers (100 in each country, except for 103 in Hungary). Teachers were older than parents (35·3 % v. 18·3 % over 45 years; P<0·001) and less likely to smoke (15·9 % v. 26·3 %, P<0·001). There was no difference between the proportions of parents and teachers who felt that a child’s physical development depended very much/extremely (v. moderately/slightly/not at all) on diet (overall 79·8 %). Lower proportions of both groups thought that mental development was very much/extremely influenced by diet (67·4 %). In the regression modelling, believing that physical and mental performance was greatly influenced by diet was significantly and positively associated with living in Hungary, scoring higher on a measure of General Health Interest and (parents only) level of education attained. Differences existed among countries in most views. Lower levels of awareness of the importance of diet for brain development and cognition (compared with physical health outcomes) indicate the potential for educating consumers, especially parents with lower educational attainment.

1. Parenchymal cells were isolated from the liver of rats that had been deprived of dietary protein for 3 weeks.

2. The cells were two-thirds the diameter of those derived from livers of normal animals and consumed oxygen at a rate of 16.2±2.7 μl/h per 106 viable cells, half the normal value.

3. Albumin and transferrin were synthesized at rates of 0.94±0.12 and 0.60±0.07 μg/h per 106 viable cells respectively and urea at a rate of 0.77±0.12 μg/h per 106 cells. This represents a 25-50% decrease in the rates of synthesis measured in cells isolated from normal livers.

4. The results are discussed in relation to the long-term effects of malnutrition on liver cell function.

The progression of cardiometabolic diseases is determined by both genetic and environmental factors. Gene–diet interactions may therefore be important in modulating the risks of developing metabolic diseases. The objectives were to investigate the effect of the interaction between brain-derived neurotrophic factor (BDNF) Val66Met polymorphisms and dietary insulin index (DII) and dietary insulin load (DIL) on cardiometabolic markers among diabetic patients. In this cross-sectional study, blood samples were collected from 667 patients. DIL and DII were defined using a validated FFQ. Genotyping the BDNF Val66Met polymorphism was conducted by the PCR-Restriction fragment length polymorphism (RFLP) method. Interactions between dietary indices and gene variants were evaluated using a generalised linear model. PGF2a concentrations were significantly higher among Val homozygotes than Met-allele carrier. This study revealed that, compared with individuals with the Val/Val genotype, those with the Met/Val or Met/Met genotype had lower BMI (Pinteraction = 0·04), TAG (Pinteraction = 0·04), leptin (Pinteraction = 0·01), LDL (Pinteraction = 0·04) and total cholesterol (Pinteraction = 0·01) when they consumed diets higher on the DIL index. Moreover, the highest quartile of the DIL, compared with the lowest, showed increase in waist circumference (Pinteraction = 0·02) and LDL/HDL (Pinteraction = 0·04) for Val/Val homozygotes compared with Met-allele carriers. BDNF Val66Met variants may interact with DIL and DII, thus be involved in the development of cardiometabolic risk factors. If diabetic patients with Met alleles regulate dietary intakes, they have a protective opportunity to regulate their cardiometabolic markers.

n-3 Long-chain PUFA up-regulate intestinal lipid metabolism. However, whether these metabolic effects of PUFA on intestine are mediated by AMP-activated protein kinase (AMPK) remains to be elucidated. To determine the effects of α-linolenic acid (ALA) on intestinal fatty acid (FA) metabolism and whether these effects were affected by AMPK deletion, mice deficient in the catalytic subunit of AMPKα1 or AMPKα2 and wild-type (WT) mice were fed either a high-fat diet (HF) or HF supplemented with ALA (HF-A). The results showed that ALA supplementation decreased serum TAG content in WT mice. ALA also increased mRNA expression of genes (carnitine palmitoyltransferase 1a, acyl-CoA oxidase 1, medium-chain acyl-CoA dehydrogenase, cytochrome P450 4A10 and pyruvate dehydrogenase kinase isoenzyme 4a) involved in intestinal lipid oxidation and mRNA expression of TAG synthesis-related genes (monoacylglycerol O-acyltransferase 2, diacylglycerol O-acyltransferases 1 and 2) in WT mice. Consistent with these, expression levels of phosphorylated AMPKα1 and AMPKα2 were also increased in WT mice after ALA addition. However, in the absence of either AMPKα1 or AMPKα2, ALA supplementation failed to increase intestinal lipid oxidation. In addition, no significant effects of either diet (HF and HF-A) or genotype (WT, AMPKα1–/– and AMPKα2–/–) on FA uptake in the intestine and faecal TAG output were observed. Our results suggest that AMPK is indispensable for the effects of ALA on intestinal lipid oxidation.

The objective of the present study was to assess the effects of Enterococcus sp. strain TN-3 isolated from deep seawater on inhibition of eosinophil accumulation, IgE production and active cutaneous anaphylaxis (ACA). We investigated the effects of viable and non-viable TN-3 on allergen-induced peritoneal eosinophil accumulation in mice. Viable (5·4 × 1010 colony-forming units per 60 mg) or non-viable TN-3 (60 mg) was orally administered to BALB/c mice that had been sensitised with the cedar pollen (Cryptomeria japonica) allergen. Oral administration of non-viable TN-3 was effective in suppressing eosinophil accumulation while viable TN-3 was ineffective. We also examined the dose–response relationship for non-viable TN-3 in regard to eosinophil accumulation, IgE production and ACA in allergen-primed mice. Non-viable TN-3 was orally administered at doses of 15 mg (low dose), 30 mg (medium dose) and 60 mg (high dose) to BALB/c mice that had been sensitised with cedar pollen allergen. The anti-allergic effects expressed as inhibition of eosinophil accumulation, IgE production and ACA were found at the low and high doses, but not at the medium dose. These results suggest that non-viable TN-3 exhibited anti-allergic effects at doses of 15 and 60 mg.

1. To elucidate the causal relation between leucine and the lowering of hepatic NAD content of rats fed on a leucine-excessive diet (Yamada et al. 1979), the effect of leucine on intestinal absorption of tryptophan was investigated.

2. Co-administration of [3H]tryptophan and leucine, with leucine at ten times the level of tryptophan, delayed absorption of L-[side chain 2,3-3H]tryptophan from the digestive tract and incorporation of [3H]tryptophan into portal blood, the liver and a protein fraction of the liver. After 120 min, more than 95% of tryptophan was absorbed whether [3H]tryptophan was administered with or without leucine.

3. Co-administration of a mixture of ten essential amino acids, in proportions simulating casein, with [3H]tryptophan markedly delayed absorption of tryptophan from the digestive tract. The addition of supplementary leucine to the amino acid mixture, however, caused no further delay.

4. In rats prefed a leucine-excessive diet for 1 week [3H]tryptophan was absorbed at the same rate as in rats fed on a control diet.

5. The results indicate that competition between tryptophan and leucine for intestinal absorption did not cause lowering of hepatic NAD.

Very little evidence exists concerning the effects of conjugated linoleic acid (CLA) on body fat reduction induced by energy restriction. Moreover, although an effect of trans-10, cis-12-CLA on lipolysis has been suggested, it has not been consistently shown. The aims of the present study were to determine whether trans-10, cis-12-CLA increases the reduction of body fat induced by energy restriction, and to analyse its effect on lipolysis and adipose tissue lipase expression (hormone-sensitive lipase (HSL) and adipose tissue TAG lipase (ATGL)). Male Syrian Golden hamsters were fed a high-fat diet during 7 weeks in order to make them fatter. Then they were submitted to a mild energy restriction (25 %) without or with supplementation of 0·5 % trans-10, cis-12-CLA for 3 weeks. Basal glycerol release and lipolysis stimulated by several drugs acting at different levels of the lipolytic cascade were measured in epididymal adipose tissue. The expression of HSL and ATGL was assessed by real-time RT-PCR. No differences were found in adipose tissues size between the experimental groups. Medium adipocyte size and total number of adipocytes were similar in both experimental groups. Animals fed the CLA-enriched diet showed similar lipolytic rates as well as HSL and ATGL expressions to the controls. In conclusion, trans-10, cis-12-CLA does not promote adipose tissue lipid mobilisation nor does it heighten body fat reduction induced by energy restriction. Consequently, this CLA isomer does not seem to be a useful tool to be included in body weight-loss strategies followed in obesity treatment.

Childbearing decreases HDL-cholesterol, potentially contributing to the increased risk of CVD in parous women. Large HDL particles (HDL-P) are associated with lower risk of CVD. In this secondary analysis of a randomised controlled trial, we investigated the effects of 12-week dietary and exercise treatments on HDL-P subclass concentration, size and apoA1 in lactating women with overweight/obesity. At 10–14 weeks postpartum, 68 women with pre-pregnant BMI 25–35 kg/m2 were randomised to four groups using 2 × 2 factorial design: (1) dietary treatment for weight loss; (2) exercise treatment; (3) both treatments and (4) no treatment. Lipoprotein subclass profiling by NMR spectroscopy was performed in serum at randomisation and after 3 and 12 months, and the results analysed with two-way ANCOVA. Lipid concentrations decline naturally postpartum. At 3 months (5–6 months postpartum), both diet (P = 0·003) and exercise (P = 0·008) reduced small HDL-P concentration. Concurrently, exercise limited the decline in very large HDL-P (P = 0·002) and the effect was still significant at 12 months (15 months postpartum) (P = 0·041). At 12 months, diet limited the decline in very large HDL-P (P = 0·005), large HDL-P (P = 0·001) and apoA1 (P = 0·002) as well as HDL size (P = 0·002). The dietary treatment for weight loss and the exercise treatment both showed effects on HDL-P subclasses in lactating women with overweight and obesity possibly associated with lower CVD risk. The dietary treatment had more effects than the exercise treatment at 12 months, likely associated with a 10 % weight loss.

The vitamin B group, including riboflavin, plays paramount roles in one-carbon metabolism (OCM), and disorders related to this pathway have been linked to cancer development. The variants of genes encoding OCM enzymes and the insufficiency of B vitamins could contribute to carcinogenesis. Very few observational studies have revealed a relationship between riboflavin and gastric cancer (GC), especially under conditions of modified genetic factors. We carried out a study examining the association of riboflavin intake and its interaction with MTRR (rs1532268) genetic variants with GC risk among 756 controls and 377 cases. The OR and 95 % CI were evaluated using unconditional logistic regression models. We observed protective effects of riboflavin intake against GC, particularly in the female subgroup (OR = 0·52, 95 % CI 0·28, 0·97, Ptrend = 0·031). In the MTRR (rs1532268) genotypes analysis, the dominant model showed that the effects of riboflavin differed between the CC and CT + TT genotypes. Compared with CC carriers, low riboflavin intake in T+ carriers was significantly associated with a 93 % higher GC risk (OR = 1·93, 95 % CI 1·09, 3·42, Pinteraction = 0·037). In general, higher riboflavin intake might help reduce the risk of GC in both CC and TC + TT carriers, particularly the T+ carriers, with marginal significance (OR = 0·54, 95 % CI 0·28, 1·02, Pinteraction = 0·037). Our study indicates a protective effect of riboflavin intake against GC. Those who carry at least one minor allele and have low riboflavin intake could modify this association to increase GC risk in the Korean population.

P ingestion has been found to alter energy balance, while regular physical exercise (E) was reported to be associated with energy compensation. However, it is not clear whether dietary P would affect energy compensation following structured E. Two experiments were performed, low P (LP) (0·1, 0·2 and 0·3 %P) and high P (HP) (0·3 , 0·6 and 1·2 %P) diets. In each experiment, male rats were randomly divided into three groups (n 8), in which a sedentary or a moderate-intensity exercise routine (30 min 5 d a week) was implemented. Energy intake (EI); efficiency and stores; body measures and total energy expenditure (TEEx) were monitored for 6 weeks. In the LP experiment, EI and weight gain were the lowest in the 0·1 and 0·2 %P as compared with the 0·3 %P. In the HP experiment, EI was highest in the high P (0·6 and 1·2 %P) groups, while weight gain was reduced. In both experiments, exercise was able to reduce body fat accumulation and to maintain a higher % lean body mass. In the LP diets experiment, the similarity in TEEx between the sedentary and exercising groups suggests the probability of a reduction in normal daily activities, which indicates the presence of compensation for the energy expended during exercise by a subsequent reduction in EE. In contrast, the elevated TEEx in the HP exercising groups (0·6 and 1·2 %P) argue against the presence of energy compensation. In conclusion, high dietary P decreases the body’s capability to compensate for the energy deficit induced by E, consequently maintaining an elevated TEEx.

1. Young rats were given, for 9 weeks, vitamin E-deficient diets containing either 20% or 10% casein, with and without a dietary supplement of 350 ppm D-α-tocopheryl acetate. For the next 5 weeks the casein content of the low-protein diets was decreased to 7%.

2. The low-protein diets induced severe growth depression.

3. The dialuric acid-induced haemolysis test showed that the rats given the 20% casein vitamin E-deficient diet were depleted of vitamin E, but that the rate of depletion on the lowcasein diet was slower.

4. Haemoglobin levels were slightly decreased by the 10% casein diets after 9 weeks, but this difference was not found after 14 weeks, comparing 20% and 7% casein. Dietary vitamin E had no effect on haemoglobin levels or erythrocyte counts.

The importance of DHA to support fetal development and maternal health is well established. In this study, we applied the natural abundance approach to determine the contribution of 200 mg/d of DHA supplement to the plasma DHA pool in nineteen healthy pregnant women. Women received DHA, from week 20 until delivery, from an algal source (n 13, Algae group) or from fish oil (n 6, Fish group) with slightly different content of 13C. We measured plasma phospholipids DHA 13C:12C ratio (reported as δ13C) prior to supplementation (T0), after 10 (T1) and 90 days (T2) and prior to delivery (T3). The δ13C of DHA in algae and fish supplements were −15·8 (sd 0·2) mUr and −25·3 (sd 0·2) mUr (P < 0·001). DHA δ13C in the Algae group increased from −27·7 (sd 1·6) mUr (T0) to −21·9 (sd 2·2) mUr (T3) (P < 0·001), whereas there were not significant changes in the Fish group (–27·8 (sd 0·9) mUr at T0 and −27·3 (sd 1·1) mUr at T3, P = 0·09). In the Algae group, 200 mg/d of DHA contributed to the plasma phospholipid pool by a median value of 53 % (31–75 % minimum and maximum). This estimation was not possible in the Fish group. Our results demonstrate the feasibility of assessing the contribution of DHA from an algal source to the plasma DHA pool in pregnant women by the natural abundance approach. Plasma δ13C DHA did not change when consuming DHA of fish origin, with almost the same δ13C value of that of the pre-supplementation plasma δ13C DHA.