Hyperuricaemia is one of the components of metabolic syndrome. Both oxidative stress and hyperinsulinism are important variables in the genesis of this syndrome and have a close association with uric acid (UA). We evaluated the effect of an oral glucose challenge on UA concentrations. The study included 656 persons aged 18 to 65 years. Glycaemia, insulin, UA and plasma proteins were measured at baseline and 120 min after an oral glucose tolerance test (OGTT). The baseline sample also included measurements of total cholesterol, triacylglycerol (TAG) and HDL-cholesterol. Insulin resistance was calculated with the homeostasis model assessment. UA levels were significantly lower after the OGTT (281·93 (sd 92·19) v. 267·48 (sd 90·40) μmol/l; P < 0·0001). Subjects with a drop in UA concentrations >40·86 μmol/l (>75th percentile) had higher plasma TAG levels (P = 0·0001), baseline insulin (P = 0·02) and greater insulin resistance (P = 0·034). Women with a difference in plasma concentrations of UA above the 75th percentile had higher baseline insulin levels (P = 0·019), concentration of plasma TAG (P = 0·0001) and a greater insulin resistance index (P = 0·029), whereas the only significant difference in men was the level of TAG. Multiple regression analysis showed that the basal TAG levels, insulin at 120 min, glycaemia at 120 min and waist:hip ratio significantly predicted the variance in the UA difference (r2 0·077). Levels of UA were significantly lower after the OGTT and the individuals with the greatest decrease in UA levels are those who have greater insulin resistance and higher TAG levels.

1. This report explores the characteristics that influenced median intakes of energy and ten nutrients in a representative sample of 1055 adolescents (11–16 years) in Tasmania, Australia.

2. Among girls, the characteristic with greatest influence on intakes was different for different nutrients. Thus, median intakes of fat, iron, thiamin and niacin-equivalent were lower in heavier, fatter girls. Girls from larger families consumed more riboflavin, while girls with poorly educated mothers consumed less vitamin A. Girls who regularly took vitamin supplements had higher median intakes of (food-derived) calcium.

3. Among boys the increase of intakes of energy and nutrients with age overshadowed the influence of other characteristics.

4. Among younger boys the characteristic with greatest influence varied. Those with highly educated fathers had lower median intakes of energy and carbohydrate; those who exercised vigorously consumed more fat; those who smoked ‘heavily’ (> 10 cigarettes in the previous week) consumed more thiamin and niacin-equivalent.

5. Among older boys the characteristic with greatest influence varied. Those who drank ‘heavily’ (> five glasses in the previous week) had higher intakes of energy and fat. Those from professional–managerial households consumed more thiamin.

6. For vitamin C, there was no sex difference in intakes. Social status had the greatest influence, with children from professional–managerial households eating more.

7. Food choices underlying these differences in energy and nutrient intakes were explored.

Synthetic α-tocopherol has eight isomeric configurations including four 2R (RSS, RRS, RSR, RRR) and four 2S (SRR, SSR, SRS, SSS). Only the RRR stereoisomer is naturally synthesised by plants. A ratio of 1·36:1 in biopotency of RRR-α-tocopheryl acetate to all-rac-α-tocopheryl acetate is generally accepted; however, studies indicate that neither biopotency of α-tocopherol stereoisomers nor bioavailability between them is constant, but depend on dose, time, animal species and organs. A total of forty growing young male mink were, after weaning, assigned one of the following treatments for 90 d: no α-tocopherol in diet (ALFA_0), 40 mg/kg RRR-α-tocopheryl acetate (NAT_40), 40 mg/kg all-rac-α-tocopheryl acetate (SYN_40) and 80 mg/kg feed all-rac-α-tocopheryl acetate (SYN_80). Mink were euthanised in CO2 and blood was collected by heart puncture. Mink were pelted and liver, heart, lungs, brain and abdominal fat were collected for α-tocopherol stereoisomer analysis. The proportion of RRR-α-tocopherol decreased in all organs and plasma with increasing amount of synthetic α-tocopherol stereoisomers in the diet (P≤0·05), whereas the proportion of all synthetic α-tocopherol stereoisomers increased with increasing amount of synthetic α-tocopherol stereoisomers in the diet (P≤0·05). The proportion of α-tocopherol stereoisomers in plasma, brain, heart, lungs and abdominal fat showed the following order: RRR>RRS, RSR, RSS>Σ2S, regardless of α-tocopherol supplement. The liver had the highest proportion of Σ2S stereoisomers, and lowest proportion of RRR-α-tocopherol. In conclusion, distribution of α-tocopherol stereoisomers differs with dose and form of α-tocopherol supplementation. The results did also reveal the liver’s role as the major organ for accumulation of Σ2S α-tocopherol stereoisomers.

Antisecretory factor (AF) is expressed in all tissues of mammals, inhibits intestinal hypersecretion and has anti-inflammatory properties as well. Endogenous AF synthesis may be stimulated by feeding hydrothermally processed cereals. Alternatively, freeze-dried egg yolk can be used as a source of exogenous AF. Several reports have suggested that AF from freeze-dried egg yolk may be useful in inflammatory bowel disease. We assessed the effect of freeze-dried, AF-rich egg yolk intake on 2,4,6-trinitrobenzenesulphonic acid (TNBS) colitis. Balb/c mice were randomised to receive (1) AF in sterile drinking-water (4 g/l, n 38) and (2) sterile drinking-water alone (vehicle, n 38) from TNBS or saline administration onwards. Different subsets of mice were killed at weeks 1–3 after TNBS or saline administration. Macroscopic and microscopic damage was assessed in colonic specimens. Eicosanoid and cytokine production was evaluated in supernatants of 24 h-incubated colonic explants. Myeloperoxidase activity was measured in frozen colonic samples, while apoptosis was assessed in paraffined samples by the in situ oligoligation method. AF-treated mice showed a milder colonic damage compared with the vehicle group, which became statistically significant at week 3. This was accompanied by decreased IL-2, IL-1 and leukotriene B4 production at weeks 2 and 3, as well as increased interferon-γ at week 1, in AF-treated mice compared with vehicle-treated mice. AF-treated mice had significantly increased counts of apoptotic cells in the lamina propria at weeks 1 and 2 post-TNBS. In conclusion, the administration of AF-rich egg yolk has a therapeutic effect in the late phases of TNBS colitis in Balb/c mice.

The influence of dietary copper on lipid composition, phospholipid-fatty acid and protein profiles and fluidity of the erythrocyte membranes of rats is reported. In general Cu deficiency in rats induced some changes in the phospholipid-fatty acid profile of erythrocyte membranes when compared with Cu-adequate animals. Stearic (18:0) and docosadienoic (22:2n-3) acids contents, for example, were significantly increased (P < 0.001) while oleic (18:1n-9) and linolenic (18:3n-3) acid contents were significantly depressed (P < 0.001) as a result of Cu deficiency. Moreover the cholesterol:phospholipids molar ratio and the cholesterol (mol):membrane proteins (mg) ratio in Cu-deficient rats were, to different degrees, significantly lower than in animals fed on Cu-adequate diets. In addition, diets deficient in Cu led to a reduction in erythrocyte membrane fluidity (P < 0.001) as assessed by the intramolecular excimer fluorescence of 1,3-di(1-pyrenyI) propane. However, no significant alteration in the phospholipid:protein ratio was observed as a result of differences in dietary treatment. The pattern of erythrocyte membrane proteins obtained with sodium dodecyl sulphate-polyacrylamide gel electro-phoresis did not seem to be influenced by Cu-deficient diets.

The increased prevalence and adverse health consequences of obesity have made it one of the leading public health issues in recent years. Importantly, several epidemiological studies have revealed significant associations between BMI and organic food consumption. However, although these studies have suggested that this factor holds promise to prevent obesity, they all suffer from methodological limitations, including self-reporting methods to assess BMI, not controlling for potential confounding factors or using a non-representative sample. Moreover, all were restricted to an adult sample. We present the results of a cross-sectional epidemiological study assessing the association of organic food consumption with BMI and obesity in a representative lifespan French sample (INCA3 study). Objective methods were used to measure BMI, and several potentially confounding variables were controlled for. In total, 1775 children and adolescents and 2121 adults underwent anthropometric measurements and completed questionnaires concerning their dietary habits and lifestyle. Unadjusted models systematically revealed negative associations between organic food consumption and both BMI and obesity across all age groups. These associations tended to remain statistically significant even after controlling for several confounding variables concerning socio-economic status, quality of the diet and physical activity. The effect sizes were, however, small. These data confirm the association between organic food consumption and obesity during both childhood and adulthood. Evidence from randomised controlled trials is required to investigate causality between organic food consumption and lower BMI or obesity rate.

Iodine nutrition is commonly assessed from iodine excretion in urine. A 24 h urine sample is ideal, but it is cumbersome and inconvenient. Hence, spot urine samples with creatinine to adjust for differences in void volume are widely used. Still, the importance of ethnicity and the timing of spot urine samples need to be settled. We, thus, collected 104 early morning spot urine samples and 24 h urine samples from Inuit and non-Inuit living in Greenland. Diet was assessed by a FFQ. Demographic data were collected from the national registry and by questionnaires. Iodine was measured using the Sandell–Kolthoff reaction, creatinine using the Jaffe method and para-amino benzoic acid by the HPLC method for the estimation of completeness of urine sampling and compensation of incomplete urine samples to 24 h excretion. A population-based recruitment was done from the capital city, a major town and a settlement (n 36/48/20). Participants were seventy-eight Inuit and twenty-six non-Inuit. The median 24 h iodine excretion was 138 (25th–75th percentile 89–225) μg/97 (25th–75th percentile 72–124) μg in Inuit/non-Inuit (P= 0·030), and 153 (25th–75th percentile 97–251) μg/102 (25th–75th percentile 73–138) μg (P= 0·026) when including compensated iodine excretion. Iodine excretion in 24 h urine samples increased with a rising intake of traditional Inuit foods (P= 0·005). Iodine excretion was lower in morning spot urine samples than in 24 h urine samples (P< 0·001). This difference was associated with iodine intake levels (P< 0·001), and was statistically significant when the iodine excretion level was above 150 μg/24 h. In conclusion, the iodine intake level was underestimated from morning spot urine samples if iodine excretion was above the recommended level.

Enterohepatic circulation of 12α-hydroxylated (12αOH) bile acid (BA) is enhanced depending on the energy intake in high-fat diet-fed rats. Such BA metabolism can be reproduced using a diet supplemented with cholic acid (CA), which also induces simple steatosis, without inflammation and fibrosis, accompanied by some other symptoms that are frequently observed in the condition of non-alcoholic fatty liver in rats. We investigated whether supplementation of the diet with raffinose (Raf) improves hepatic lipid accumulation induced by the CA-fed condition in rats. After acclimation to the AIN-93-based control diet, male Wistar rats were fed diets supplemented with a combination of Raf (30 g/kg diet) and/or CA (0·5 g/kg diet) for 4 weeks. Dietary Raf normalised hepatic TAG levels (two-way ANOVA P < 0·001 for CA, P = 0·02 for Raf and P = 0·004 for interaction) in the CA-supplemented diet-fed rats. Dietary Raf supplementation reduced hepatic 12αOH BA concentration (two-way ANOVA P < 0·001 for CA, P = 0·003 for Raf and P = 0·03 for interaction). The concentration of 12αOH BA was reduced in the aortic and portal plasma. Raf supplementation increased acetic acid concentration in the caecal contents (two-way ANOVA P = 0·001 as a main effect). Multiple regression analysis revealed that concentrations of aortic 12αOH BA and caecal acetic acid could serve as predictors of hepatic TAG concentration (R2 = 0·55, P < 0·001). However, Raf did not decrease the secondary 12αOH BA concentration in the caecal contents as well as the transaminase activity in the CA diet-fed rats. These results imply that dietary Raf normalises hepatic lipid accumulation via suppression of enterohepatic 12αOH BA circulation.

Fructose-rich diets (FRD) cause cardiac insulin resistance manifested by impairment of Akt/endothelial NO synthase (eNOS) signalling. In contrast, oestradiol (E2) activates this signalling pathway in the heart. To study the ability of E2 to revert the detrimental effect of fructose on cardiac Akt/eNOS, female rats were subjected to a FRD and ovariectomy followed with or without E2 replacement. We also analysed the effects of the FRD and E2 on cardiac extracellular signal-regulated kinase (Erk 1/2) signalling related to their role in cardiac hypertrophy development. Expression of Akt, eNOS and Erk 1/2, as well as regulatory phosphorylations of these molecules were determined. The protein expression of cardiac Akt and eNOS was not affected by the diet or E2 treatment. However, the FRD was accompanied by a decrease in Akt phosphorylation at Ser473 and Thr308, and eNOS at Ser1177, while the phosphorylation of eNOS at Thr495 was increased. E2 replacement in ovariectomised fructose-fed rats caused a reversion of the diet effect on Akt and eNOS serine phosphorylation, but mostly had no effect on threonine phosphorylation of the molecules. The FRD and E2 treatment did not influence Erk 1/2 expression and phosphorylation and heart mass as well. The data show that E2 selectively suppress the negative effects of a FRD on Akt/eNOS signalling and probably point to the different effects of E2 on kinase/phosphatase pathways responsible for phosphorylation/dephosphorylation of Akt and eNOS. Furthermore, the results suggest that the heart of females in the reproductive period is partially protected against the damaging effects of increased fructose intake.

Previous nutritional studies have shown that insulin regulation is different between DT and A strains of gibel carp. As leptin plays a pivotal role in the effects of insulin, we hypothesised that leptin regulation of glucose and lipid metabolism would differ between the two strains. To test our hypothesis, recombinant human leptin was injected into two strains. The results showed that leptin activated the phosphatidylinositol 3-kinase (PI3K)–protein kinase B (AKT), AMP-activated protein kinase–acetyl coenzyme A carboxylase and Janus kinase 2 (JAK2)–signal transducer and activator of transcription (STAT) signalling pathways in both strains. Hypoglycaemia induced by leptin might be due to higher glucose uptake by the liver and muscles together with enhanced glycolytic potential and reduced gluconeogenic potential. Decreased lipogenesis and up-regulated fatty acid oxidation were induced by leptin. In terms of genotype, the PI3K–AKT signalling pathway was more strongly activated by leptin in the muscle tissue of the A strain, as reflected by the heightened phosphorylation of AKT. Furthermore, glycogen content, glycolytic enzyme activity and gluconeogenic capability were higher in the A strain than the DT strain. Strain A had higher levels of fatty acid synthesis and lipolytic capacity in the liver than the DT strain, but the opposite was true in white muscle. Regarding leptin–genotype interactions, the DT strain displayed stronger regulation of glucose metabolism in the liver by leptin as compared with the A strain. Moreover, a more active JAK2–STAT signalling pathway accompanied by enhanced inhibition of fatty acid synthesis by leptin was observed in the DT strain. Overall, the regulation of glucose and lipid metabolism by leptin differed between the two strains, as expected.

Breast milk composition varies with maternal factors including diet and confers health benefits to the neonate; however, the mechanisms mediating this protection remain incompletely understood. Our aim was to investigate the effects of supplementing a maternal high-fat/sucrose (HFS) diet with prebiotic oligofructose (OFS) on milk composition in rats and associations with offspring body composition and gut microbiota. Obese Sprague–Dawley dams consumed a control, HFS, HFS + OFS (10 % wt/wt) or HFS diet weight-matched to the HFS + OFS group (HFS-WM) during pregnancy and lactation. Pups were weaned onto a HFS diet on day 21. Milk was collected at weaning and analysed for protein, leptin and microRNA (miRNA) levels. Milk produced by HFS dams contained less protein than milk from lean controls which was normalised by OFS. Six miRNA (miR-222, miR-203a, miR-200a, miR-26a, miR-27a and miR-103) were differentially expressed in milk according to maternal diet. Milk leptin content was positively correlated with maternal body fat and faecal Enterobacteriaceae in male offspring at 24 weeks of age. Milk protein content was inversely associated with maternal body fat and body weight. miR-200a was positively associated with maternal body fat and Enterobacteriaceae in female offspring at 24 weeks of age. Correlations between milk protein and multiple milk miRNA and offspring body composition and gut microbiota differed by sex. Overall, our results suggest that obesogenic diets and prebiotic supplementation can alter the protein and miRNA levels in breast milk in rats and these milk components may explain, in part, the influence of these maternal diets on offspring body composition.

In humans, maximum brain development occurs between the third trimester of gestation and 2 years of life. Nutrition during these critical windows of rapid brain development might be essential for later cognitive functioning and behaviour. In the last few years, trends on protein recommendations during infancy and childhood have tended to be lower than that in the past. It remains to be demonstrated that lower protein intakes among healthy infants, a part of being able to reduce obesity risk, is safe in terms of mental performance achievement. Secondary analyses of the EU CHOP, a clinical trial in which infants from five European countries were randomised to be fed a higher or a lower protein content formula during the 1st year of life. Children were assessed at the age of 8 years with a neuropsychological battery of tests that included assessments of memory (visual and verbal), attention (visual, selective, focused and sustained), visual-perceptual integration, processing speed, visual-motor coordination, verbal fluency and comprehension, impulsivity/inhibition, flexibility/shifting, working memory, reasoning, visual-spatial skills and decision making. Internalising, externalising and total behaviour problems were assessed using the Child Behaviour Checklist 4–18. Adjusted analyses considering factors that could influence neurodevelopment, such as parental education level, maternal smoking, child’s gestational age at birth and head circumference, showed no differences between feeding groups in any of the assessed neuropsychological domains and behaviour. In summary, herewith we report on the safety of lower protein content in infant formulae (closer to the content of human milk) according to long-term mental performance.

The adverse effect of red meat consumption on the risk for CVD is a major population health concern, especially in developing Hispanic/Latino countries in which there are clear trends towards increased consumption. This population-based case–control study examined the associations between total, processed and unprocessed red meat intakes and non-fatal acute myocardial infarction (MI) in Costa Rica. The study included 2131 survivors of a first non-fatal acute MI and 2131 controls individually matched by age, sex and area of residence. Dietary intake was assessed with a FFQ. OR were estimated by using conditional logistic regression. Higher intakes of total and processed red meat were associated with increased odds of acute MI. The OR were 1·31 (95 % CI 1·04, 1·65) and 1·29 (95 % CI 1·01, 1·65) for the highest quintiles of total red meat (median: 110·8 g or 1 serving/d) and processed red meat intake (median: 36·1 g or 5 servings/week), respectively. There were increasing trends in the odds of acute MI with higher total (P trend=0·01) and processed (P trend=0·02) red meat intakes. Unprocessed red meat intake was not associated with increased odds of acute MI. Substitutions of 50 g of alternative foods (fish, milk, chicken without skin and chicken without fat) for 50 g of total, processed and unprocessed red meat were associated with lower odds of acute MI. The positive association between red meat intake and acute MI in Costa Rica highlights the importance of reducing red meat consumption in middle-income Hispanic/Latino populations.