Despite Fe deficiency and overload having been widely studied, no studies are available about the influence of milk consumption on antioxidant defence and lipid peroxidation during the course of these highly prevalent cases. The objective of the present study was to assess the influence of cow or goat milk-based diets, either with normal or Fe-overload, on antioxidant defence and lipid peroxidation in the liver, brain and erythrocytes of control and anaemic rats after chronic Fe repletion. Weanling male rats were randomly divided into two groups: a control group receiving a normal-Fe diet (45 mg/kg) and an anaemic group receiving a low-Fe diet (5 mg/kg) for 40 d. Control and anaemic rats were fed goat or cow milk-based diets, either with normal Fe or Fe-overload (450 mg/kg), for 30 or 50 d. Fe-deficiency anaemia did not have any effect on antioxidant enzymes or lipid peroxidation in the organs studied. During chronic Fe repletion, superoxide dismutase (SOD) activity was higher in the group of animals fed the cow milk diet compared with the group consuming goat milk. The slight modification of catalase and glutathione peroxidise activities in animals fed the cow milk-based diet reveals that these enzymes are unable to neutralise and scavenge the high generation of free radicals produced. The animals fed the cow milk diet showed higher rates of lipid peroxidation compared with those receiving the goat milk diet, which directly correlated with the increase in SOD activity. It was concluded that goat milk has positive effects on antioxidant defence, even in a situation of Fe overload, limiting lipid peroxidation.

A total of four barren adult female muskoxen (Ovibos moschatus) were used over a period of 2 years for the purpose of the present study. During the first year, the natural changes in appetite (ad libitum intake of standard pelleted reindeer feed) and body mass were determined in two of the animals. During the second year, the effect of reduced food quality on ad libitum food intake was tested in all four animals in July when the appetite had been found to be at a high. We found that the experimentally reduced food quality was not compensated with increased food intake in these large high-Arctic herbivores.

Fe bioavailability can be manipulated by the nutritional composition of a meal. Ascorbic acid and unidentified components of meat, fish and poultry, but particularly beef, all appear to enhance the absorption of non-haem Fe. The aim of the present study is to identify whether extracts of green-lipped mussels (GLM; Perna canaliculus) enhance non-haem Fe absorption in Caco-2 cells and to compare the effect with that of beef. Raw GLM and raw beef homogenates were digested in vitro with pepsin at pH 2, and pancreatin and bile salts at pH 7. Tracer 55Fe was used to measure cellular Fe uptake. Ascorbic acid was used as a positive control and egg albumin, exposed to the same in vitro digestion process, was used as a negative control. Caco-2 cell monolayers were incubated with treatments for 60 min. All values were standardised per μg of GLM, egg albumin, beef or ascorbic acid. The results showed that ascorbic acid enhanced non-haem Fe absorption to the highest degree. Beef and GLM digestates both significantly enhanced Fe absorption compared with egg albumin. In conclusion, GLM digestate significantly enhances non-haem Fe uptake in Caco-2 cells with a similar magnitude to that of beef.

The peptide hormone hepcidin functions as a negative regulator of intestinal Fe absorption and Fe recycling. Since its discovery as a systemic negative regulator of Fe metabolism, hepcidin has attracted enormous interest as a potential drug for the treatment and/or prevention of several forms of Fe overload. We therefore tested whether multiple doses of intraperitoneally administered synthetic renatured hepcidin can prevent hepatic Fe loading in mice concurrently fed an Fe-rich diet, and whether the same treatment affects hepatic Fe stores in mice fed a normal diet. Cohorts of male mice were fed either a normal defined diet (180 parts per million Fe) or an Fe-rich diet (the same diet supplemented with 2 % carbonyl iron for 2 weeks). Concurrently, half of the animals in each diet group received 100 μg of renatured hepcidin intraperitoneally every 12 h, for the same 2-week period. The second half of the animals received PBS only. The renatured synthetic hepcidin demonstrated biological activity by significantly decreasing transferrin saturation, which lasted for up to 24 h after a single hepcidin dose. However, the 14 d intraperitoneal hepcidin therapy did not prevent hepatic Fe overload in mice fed the Fe-rich diet, nor did it affect hepatic Fe stores in mice fed the normal diet. Both hepcidin agonists and antagonists are expected to have broad therapeutic potential. The absence of an effect of biologically active hepcidin on hepatic Fe loading shows the need for thorough future studies on the hepcidin regulation of Fe absorption and tissue distribution.

Mammals have an endogenous timing system in the suprachiasmatic nuclei (SCN) of the hypothalamic region of the brain. This internal clock system is composed of an intracellular feedback loop that drives the expression of molecular components and their constitutive protein products to oscillate over a period of about 24 h (hence the term ‘circadian’). These circadian oscillations bring about rhythmic changes in downstream molecular pathways and physiological processes such as those involved in nutrition and metabolism. It is now emerging that the molecular components of the clock system are also found within the cells of peripheral tissues, including the gastrointestinal tract, liver and pancreas. The present review examines their role in regulating nutritional and metabolic processes. In turn, metabolic status and feeding cycles are able to feed back onto the circadian clock in the SCN and in peripheral tissues. This feedback mechanism maintains the integrity and temporal coordination between various components of the circadian clock system. Thus, alterations in environmental cues could disrupt normal clock function, which may have profound effects on the health and well-being of an individual.

The first months of life correspond to a key period in human life where dramatic physiological changes (establishment of microbiota, development of the immune system, etc.) occur. In order to better control these changes it is necessary to understand the behaviour of food in the gastrointestinal tract of the newborn. Infant formula is the only food for the newborn when breast-feeding is impossible. The kinetics of digestion of milk proteins and the nature of the peptides liberated in the small intestine throughout infant formula digestion have never been extensively investigated so far and were therefore studied using the piglet as a model of the newborn child. Piglets were fed infant formula by an automatic delivery system during 28 d, and slaughtered 30, 90 and 210 min after the last meal. Contents of stomach, proximal and median jejunum and ileum were collected and characterised. The extent of β-lactoglobulin (β-lg), α-lactalbumin (α-la) and casein proteolysis was monitored by inhibition ELISA, SDS-PAGE, immunoblotting and MS. At 30 min after the last meal, caseins were shown to be extensively hydrolysed in the stomach. Nevertheless, peptides originating mainly from β-caseins (from 509 to 2510 Da) were identified in the jejunum and ileum of the piglets. β-Lg partially resisted gastric digestion but completely disappeared in the stomach after 210 min. α-La had a similar behaviour to that of β-lg. Two large peptides (4276 and 2674 Da) generated from β-lg were present in the ileum after 30 and 210 min and only one (2674 Da) after 90 min.

High-fat diet is a major causative factor of overweight and obesity, which are associated with an increased risk of neuropsychiatric diseases, such as anxiety and depression. In the present study, we investigated the protective effects of bamboo extract (BEX) on anxiety- and depression-like neurobehaviours in mice treated with a high-fat diet. Male mice with CD-1 genetic background were treated for 2 months with either a standard or a high-fat diet (10 or 45 % energy from fat, respectively), with or without the BEX supplement (11 g dry mass per 17 MJ). The anxiety levels of mice were evaluated using open-field and hole-board tests, and depression was measured using the force-swimming test. The anxiety responses of the animals were found significantly increased after the high-fat diet treatment, and this elevation was effectively abolished by the BEX supplement. The high-fat diet seemed to have an anti-depressive effect in mice at the tested time point, but the effect of the BEX supplement on the depression level of the animals was not conclusive. The high-fat diet significantly decreased total glutathione content in the blood while the BEX supplement increased glutathione oxidation. In summary, the present study shows that decreased total glutathione concentration in the blood co-occurred with a high-fat treatment, high anxiety level and low depression level in mice, and when supplemented in a high-fat diet, BEX had an anxiolytic effect in mice.

Direct observation(s) of energy intake (EI) via buffet meals served in the laboratory are often carried out within short-term exercise intervention studies. The reproducibility of values obtained has not been assessed either under resting control conditions or post-exercise, in overweight and obese females. A total of fourteen sedentary, pre-menopausal females (BMI 30·0 (sd 5·1) kg/m2) completed four trials; two exercise and two control. Each trial lasted 24 h spanning over 2 d; conducted from afternoon on day 1 and morning on day 2. An exercise session to expend 1·65 MJ was completed on day 1 of exercise trials, and three buffet meals were served during each trial. Reproducibility of post-exercise changes in energy and macronutrient intakes was assessed at each individual buffet meal by intraclass correlation coefficient (ri). Only the ri values for post-exercise changes in energy (ri 0·44 (95 % CI − 0·03, 0·77), P = 0·03) and fat intake (ri 0·51 (95 % CI 0·04, 0·81), P = 0·02) at the lunch buffet meal achieved statistical significance; however, these ri values were weak and had large associated 95 % CI, which indicates a large degree of variability associated with these measurements. Energy and macronutrient intakes at the breakfast and evening buffet meals were not reproducible. This study concludes that the frequently used laboratory-based buffet meal method of assessing EI does not produce reliable, reproducible post-exercise changes in EI in overweight and obese women.

Using dietary fibre to control childhood diarrhoea has rarely been discussed. However, dietary fibre is being proposed to prevent diarrhoea in piglets. The present study aimed to study the effects of introducing fibre in the post-weaning piglet diet and its particle size on the intestinal ecosystem before and after an experimental infection with Escherichia coli. A total of thirty-six post-weaning piglets were assigned to four experimental diets: a negative control (NC) diet, the same diet with 4 % wheat bran coarse (WBc) particle size or finely milled (WBF) and a positive control (PC) diet with an antibiotic. On day 9, animals were challenged with E. coli. Faecal and digesta samples were obtained before and after the experimental infection and changes in the microbial ecosystem were measured. Animals fed the WBc and the PC diets showed a significant reduction in the faecal score compared with the NC diet. The inclusion of WBc in the diet increased total volatile fatty acid concentration, reduced Bacteroidetes in the faeces before and after the experimental infection compared with the NC diet and increased Firmicutes at the end of the experiment. Based on the results, diarrhoea scours and the composition of the pig gut microbial community are modified by the inclusion of a relatively small amount of wheat bran in the diet, being the physical presentation of the fibre a determinant of that difference.

The objective of the present study was to determine the effect of Se inclusion in high-DHA and vitamin E microdiets (5 g DHA/100 g dry weight and 300 mg vitamin E/100 g dry weight; 5 g DHA/100 g dry weight and 300 mg vitamin E/100 g dry weight supplemented with Se) in comparison with a control diet (1 g DHA/100 g dry weight and 150 mg vitamin E/100 g dry weight) on sea bass larval growth, survival, biochemical composition, malonaldehyde (MDA) content, muscle morphology and antioxidant enzymes (AOE), insulin-like growth factors (IGF) and myosin expression. For a given DHA and vitamin E dietary content, Se inclusion favoured larval total length and specific growth rate, and reduced the incidence of muscular lesions, MDA contents and AOE gene expression. In contrast, IGF gene expression was elevated in the 5/300 larvae, suggesting an increased muscle mitogenesis that was corroborated by the increase in mRNA copies of myosin heavy chain. The results of the present study denoted the beneficial effect of Se not only in preventing oxidative stress, as a glutathione peroxidase cofactor, but probably due to other as yet unknown physiological functions.

The present study was conducted to test the hypothesis that dietary arginine promotes digestion and absorption capacity, and, thus, enhances fish growth. This improvement might be related to the target of rapamycin (TOR) and eIF4E-binding protein (4E-BP). A total of 1200 juvenile Jian carp, Cyprinus carpio var. Jian, with an average initial weight of 6·33 (se 0·03) g, were fed with diets containing graded concentrations of arginine, namely, 9·8 (control), 12·7, 16·1, 18·5, 21·9 and 24·5 g arginine/kg diet for 9 weeks. An real-time quantitative PCR analysis was performed to determine the relative expression of TOR and 4E-BP in fish muscle, hepatopancreas and intestine. Dietary arginine increased (P < 0·05): (1) glutamate-oxaloacetate transaminase and glutamate-pyruvate transaminase activities in muscle and hepatopancreas; (2) intestine and hepatopancreas protein content, folds height, and trypsin, chymotrypsin, lipase, Na+/K+-ATPase, alkaline phosphatase, γ-glutamyl transpeptidase and creatine kinase activities in intestine; (3) Lactobacillus counts; (4) relative expression of TOR in the muscle, hepatopancreas and distal intestine (DI); (5) relative expression of 4E-BP in proximal intestine (PI) and mid-intestine (MI), as compared with the control group. In contrast, dietary arginine reduced (P < 0·05): (1) plasma ammonia content; (2) Aeromonas hydrophila and Escherichia coli counts; (3) relative expression of TOR in PI and MI; (4) relative expression of 4E-BP in the muscle, hepatopancreas and DI. The arginine requirement estimated by specific growth rate using quadratic regression analysis was found to be 18·0 g/kg diet. These results indicate that arginine improved fish growth, digestive and absorptive ability and regulated the expression of TOR and 4E-BP genes.

Vitamin D deficiency and the rapid increase in the prevalence of obesity are both considered important public health issues. The classical role of vitamin D is in Ca homoeostasis and bone metabolism. Growing evidence suggests that the vitamin D system has a range of physiological functions, with vitamin D deficiency contributing to the pathogenesis of several major diseases, including obesity and the metabolic syndrome. Clinical studies have shown that obese individuals tend to have a low vitamin D status, which may link to the dysregulation of white adipose tissue. Recent studies suggest that adipose tissue may be a direct target of vitamin D. The expression of both the vitamin D receptor and 25-hydroxyvitamin D 1α-hydroxylase (CYP27B1) genes has been shown in murine and human adipocytes. There is evidence that vitamin D affects body fat mass by inhibiting adipogenic transcription factors and lipid accumulation during adipocyte differentiation. Some recent studies demonstrate that vitamin D metabolites also influence adipokine production and the inflammatory response in adipose tissue. Therefore, vitamin D deficiency may compromise the normal metabolic functioning of adipose tissue. Given the importance of the tissue in energy balance, lipid metabolism and inflammation in obesity, understanding the mechanisms of vitamin D action in adipocytes may have a significant impact on the maintenance of metabolic health. In the present review, we focus on the signalling role of vitamin D in adipocytes, particularly the potential mechanisms through which vitamin D may influence adipose tissue development and function.

Epidemiological studies have reported a greater reduction in cardiovascular risk and metabolic disorders associated with diets rich in polyphenols. The antioxidant effects of polyphenols are attributed to the regulation of redox enzymes by reducing reactive oxygen species production from mitochondria, NADPH oxidases and uncoupled endothelial NO synthase in addition to also up-regulating multiple antioxidant enzymes. Although data supporting the effects of polyphenols in reducing oxidative stress are promising, several studies have suggested additional mechanisms in the health benefits of polyphenols. Polyphenols from red wine increase endothelial NO production leading to endothelium-dependent relaxation in conditions such as hypertension, stroke or the metabolic syndrome. Numerous molecules contained in fruits and vegetables can activate sirtuins to increase lifespan and silence metabolic and physiological disturbances associated with endothelial NO dysfunction. Although intracellular pathways involved in the endothelial effects of polyphenols are partially described, the molecular targets of these polyphenols are not completely elucidated. We review the novel aspects of polyphenols on several targets that could trigger the health benefits of polyphenols in conditions such as metabolic and cardiovascular disturbances.