Inulin is a generic term to cover all β(2 → 1) linear fructans. Chicory inulin is a linear β(2 → 1) fructan (degree of polymerisation (DP) 2 to 60; DPav = 12), its partial enzymatic hydrolysis product is oligofructose (DP 2 to 8; DPav = 4), and by applying specific separation technologies a long-chain inulin knownas inulin HP (DP 10 to 60; DPav = 25) can be produced. Finally, a specific product known as oligofructose-enriched inulin is obtained by combining chicorylong-chain inulin and oligofructose. Because of the b-configuration of the anomeric C2 in their fructose monomers, inulin-type fructans resist hydrolysis byintestinal digestive enzymes, they classify as ‘non-digestible’ carbohydrates, and they are dietary fibres. By increasing faecal biomass and water content ofthe stools, they improve bowel habits, but they have characteristic features different from other fibres. They affect gastrointestinal functions not because oftheir physico-chemical properties but rather because of their biochemical and physiological attributes. In the colon, they are rapidly fermented to produceSCFA that are good candidates to explain some of the systemic effects of inulin-type fructans. Fermentation of inulin-type fructans in the large bowel is aselective process; bifidobacteria (and possibly a few other genera) are preferentially stimulated to grow, thus causing significant changes in the compositionof the gut microflora by increasing the number of potentially health-promoting bacteria and reducing the number of potentially harmful species. Both oligofructosead inulin are prebiotic. They also induce changes in colonic epithelium stimulating proliferation in the crypts, increasing the concentration ofpolyamines, changing the profile of mucins, and modulating endocrine as well as immune functions. From a nutrition labelling perspective, inulin-typefructans are not only prebiotic dietary fibres; they are also low-calorie carbohydrates [6·3 kJ/g (1·5 kcal/g)]. Supported by the results of a large numberof animal studies and human nutrition intervention trials, the claim ‘inulin-type fructans enhance calcium and magnesium absorption‘ is scientifically substantiated, but different inulin-type fructans have probably a different efficacy (in terms of effective daily dose), the most active product being the oligofructose-enriched inulin. A series of animal studies demonstrate that inulin-type fructans affect the metabolism of lipids primarily by decreasingtriglyceridaemia because of a reduction in the number of plasma VLDL particles. The human data largely confirm the animal experiments. They demonstratemainly a reduction in triglyceridaemia and only a relatively slight decrease in cholesterolaemia mostly in (slightly) hypertriglyceridaemic conditions. Inulinappears thus eligible for an enhanced function claim related to normalization of blood triacylglycerols. A large number of animal data convincingly showthat inulin-type fructans reduce the risk of colon carcinogenesis and nutrition intervention trials are now performed to test that hypothesis in human subjectsknown to be at risk for polyps and cancer development in the large bowel.

Definitions of functional food vary but are essentially based on foods' ability to enhance the quality of life, or physical and mental performance, of regular consumers. The worldwide use of coffee for social engagement, leisure, enhancement of work performance and well-being is widely recognised. Depending on the quantities consumed, it can affect the intake of some minerals (K, Mg, Mn, Cr), niacin and antioxidant substances. Epidemiological and experimental studies have shown positive effects of regular coffee-drinking on various aspects of health, such as psychoactive responses (alertness, mood change), neurological (infant hyperactivity, Alzheimer's and Parkinson's diseases) and metabolic disorders (diabetes, gallstones, liver cirrhosis), and gonad and liver function. Despite this, most reviews do not mention coffee as fulfilling the criteria for a functional food. Unlike other functional foods that act on a defined population with a special effect, the wide use of coffee-drinking impacts a broad demographic (from children to the elderly), with a wide spectrum of health benefits. The present paper discusses coffee-drinking and health benefits that support the concept of coffee as a functional food.

The extent to which maternal folate and vitamin B12 modulate infant birth weight is unclear. The present study investigated mothers in early gestation (mean 11·5 (sd 5·8) weeks) and neonates, at delivery. Erythrocyte (RBC) folate (mothers: n 683; neonates: n 614) and vitamin B12 (mothers: n 534; neonates: n 614) were measured. Data on smoking habits were available for 44 % of pregnancies (n 443). The relationship between vitamin levels and birth weight standardized for gender and gestational age was investigated, using linear regression and adjusting for possible confounding variables (maternal age, parity). Results are presented as standardized regression coefficients (b). Increasing maternal age was associated with elevated RBC folate (b 0·11 (95 % CI 0·08, 0·15), P<0·001; n 674) and smoking was associated with a decrease in maternal RBC folate (b −1·38 (95 % CI −1·92, −0·86), P=0·001; n 319). Neonatal RBC folate was predicted by maternal RBC folate (b 0·08 (95 % CI 0·04, 0·11), P=0·001; n 315) and maternal vitamin B12 (b 0·08 (95 % CI 0·01, 0·16), P=0·02; n 252). Smoking influenced maternal vitamin B12 status (b −0·88 (95 % CI −1·49, −0·27), P=0·005; n 231). Using univariate regression, smoking significantly influenced infant birth weight (b −2·15 (95 % CI −3·24, −1·04), P<0·001; n 437). However, the effect of smoking on birth weight was statistically non-significant when considered in a multivariate regression model, leaving maternal RBC folate as the only significant predictor of birth weight (b 0·25 (95 % CI 0·08, 0·42), P=0·005; n 145). These findings suggest that maternal folate status is an important determinant of infant birth weight. The combined effects of smoking and reduced RBC status on birth weight require further investigation.

The behavioural and cognitive effects of oligofructose-enriched inulin at the doses of 5 and 10% in the diet, orally ingested daily during 2 weeks, wereinvestigated using a functional observational battery (FOB) and the light extinction test in male Wistar rats. Control rats received a standard diet and were tested in the same test situations. The behavioural effects were assessed 2 d before and 14 d after the beginning of the treatment period and the cognitive effects were investigated after the administration period by lever-pressing activity and learning discrimination using the light extinction test paradigm. In general, the study demonstrated that oligofructose-enriched inulin at 5% in the diet, and particularly at 10% in the diet, caused relaxing-like effects, stimulated and increased the general activity and interest of the rats to the test environment. In addition, both doses of oligofructose-enriched inulin showed significant effects on learning discrimination in male rats, in comparison with the control diet. These results suggest that oligofructose-enriched inulin, particularly at the dose of 10 %, improves cognitive performances in the light extinction test and the well-being of male rats using the FOB.

Anti-angiogenic strategies are emerging as an important tool for the treatment of cancer and inflammatory diseases. In the present investigation we isolated several isoflavones from a tempeh (fermented soyabean) extract. The isolated isoflavones were identified as 5,7,4′-trihydroxyisoflavone (genistein), 7,4′-dihydroxyisoflavone (daidzein), 6,7,4′-trihydroxyisoflavone (factor 2), 7,8,4′-trihydroxyisoflavone (7,8,4′-TriOH) and 5,7,3′,4′-tetrahydroxyisoflavone (orobol). The effects on angiogenesis of these isoflavones were evaluated in the chicken chorioallantoic membrane assay; their capacity to inhibit vascular endothelial growth factor-induced endothelial cell proliferation and expression of the Ets 1 transcription factor, known to be implicated in the regulation of new blood vessel formation, were also investigated. We found that all isoflavones inhibited angiogenesis, albeit with different potencies. Compared with negative controls, which slightly inhibited in vivo angiogenesis by 6·30 %, genistein reduced angiogensis by 75·09 %, followed by orobol (67·96 %), factor 2 (56·77 %), daidzein (48·98 %) and 7,8,4′-TriOH (24·42 %). These compounds also inhibited endothelial cell proliferation, with orobol causing the greatest inhibition at lower concentrations. The isoflavones also inhibited Ets 1 expression, providing some insight into the molecular mechanisms of their action. Furthermore, the chemical structure of the different isoflavones suggests a structure–activity relationship. Our present findings suggest that the new isoflavones might be added to the list of low molecular mass therapeutic agents for the inhibition of angiogenesis.

Conjugated linolenic acid (CLN) refers to a group of octadecatrienoic acid isomers that have three double bonds in conjugation. Both pomegranate and tung seed oils are rich in CLN but the major isomer in the former is cis9,trans11,cis13 while in the latter it is cis9,trans11,trans13. The present study examined the effects of CLN, isolated from either pomegranate seed oil or tung seed oil, and α-linolenic acid (LN), isolated from flaxseed oil, on serum cholesterol levels in male hamsters (body weight 105 g; age 10 weeks) fed a 0.1 % cholesterol and 10 % lard diet, for a period of 6 weeks. All hamsters were allowed free access to food and fluid. The blood samples were taken by bleeding from the retro-orbital sinus into a heparinized capillary tube under light ether anaesthesia after overnight fasting at weeks 0, 2, 4 and 6. It was found that supplementation of CLN at levels of 12.2–12.7 g/kg diet exhibited no significant effect on serum cholesterol level while LN at a similar level of supplementation had serum cholesterol reduced by 17–21 % compared with the control diet containing no LN and CLN. Supplementation of CLN and LN significantly decreased hepatic cholesterol but no effect was observed on heart and kidney cholesterol levels. It was concluded that LN possessed hypocholesterolaemic activity while CLN had no effect on blood cholesterol, at least in hamsters.

Recent studies have shown an inverse association between the level of dietary Ca, particularly from dairy sources, and body weight in adults; there is, however, a paucity of data regarding this relationship in children. We therefore investigated this issue in 1087 children who underwent body weight and height measurement during a survey on childhood obesity. Lifestyle and dietary habits were investigated by a questionnaire. After excluding children who were following a dietary regimen for any reason, 884 children (M:F 451:433; age 7·5 (sd 2·1) years) were selected. Milk consumption was pooled into four frequency categories: poor (≤1/week; n 125), moderate (>1 but ≤5–6/week; n 133), regular (1/d; n 408) and high (≥2/d; n 218). The frequency of consumption of milk was inversely and significantly associated (t=–2·64, P=0·003) with age- and sex-specific BMI z-scores by linear regression analysis, controlling for sex, age, physical activity, birth weight and parental overweight and education. The statistical association remained significant (t=–2·831, P=0·005) after the inclusion of children consuming only skimmed milk (n 91). Milk consumption was still significantly and inversely associated with BMI z score (t=–2·791, P=0·005) in the whole-milk consumers when controlling for age and the frequency of consumption of various foods; this association was no longer significant (P=0·21) when children consuming skimmed milk were included in the analysis. This is the first report showing a significant inverse association between frequency of milk consumption and body mass in children. Regardless of the mechanisms involved, our results might encourage further research on this issue and might have important implications for the prevention of obesity.

Transgenic mice that overexpress arginase-I in their small-intestinal enterocytes suffer from a pronounced, but selective decrease in circulating arginine levels during the suckling period, resulting in impaired growth and development of hair, muscle and immune system. In the present study, we tested the hypothesis that the arginine-deficiency phenotype is caused by arginine-specific post-translational modifications, namely, an increase in the degree of mono-ADP-ribosylation of proteins because of reduced competition by free arginine residues and/or an increase in protein-tyrosine nitration because of an increased O2− production by NO synthases in the presence of limiting amounts of arginine. Arginine ADP-ribosylation and tyrosine nitration of proteins in the affected organs were assayed by Western blot analysis, using specific anti-ADP-ribosylarginine and protein-nitrotyrosine antisera. The composition of the group of proteins that were preferentially arginine ADP-ribosylated or tyrosine-nitrated in the respective organs was strikingly similar. Arginine-deficient mice differed from their controls in a reduced ADP-ribosylation of a 130 kDa and a 65 kDa protein in skin and an increased protein nitration of an 83 kDa protein in bone marrow and a 250 kDa protein in spleen. Since only 20 % of the visualised proteins were differentially modified in a subset of the affected organs, our findings appear to rule out these prominent arginine-dependent post-translational protein modifications as mediators of the characteristic phenotype of severely arginine-deficient mice.

The aim of this study was to determine whether dietary supplementation with branched-chain amino acids, and the infusion of insulin and dextrose, would increase milk protein secretion in the sow. The experiment involved sixteen lactating sows fed either a normal lactation diet (162 g/kg crude protein, n 8) or a high-protein diet (230 g/kg crude protein, n 8) supplemented with branched-chain amino acids (valine, isoleucine and leucine). Sows were either infused with insulin and dextrose or not infused at all during mid (day 5–10) and late (day 17–22) lactation in a single reversal design. Blood samples were analysed for glucose, and the dextrose infusion rate was adjusted to maintain the blood glucose level within 15 % of pre-infusion levels. Milk (10·1 v. 11·1 kg/d; P=0·014) and\ lactose (628 v. 727 g/d; P=0·002) yield increased with insulin infusion, whereas milk protein content (5·0 % v. 5·5 %; P=0·007) was increased in diets supplemented with protein and branched-chain amino acids. Piglet growth was increased by feeding the higher-protein diet (237 v. 273 g/d; P=0·05) but not significantly increased by insulin infusion (245 v. 265 g/d; P=0·11). These effects were additive such that the combined treatment resulted in a 24 % (56 g/d; P<0·05) increase in piglet growth rate. These data demonstrate that increasing the dietary protein/branched-chain amino acid content can increase milk protein secretion but not milk yield. The infusion of insulin and dextrose increased milk and milk lactose yields, and tended to increase milk protein yield but not milk protein content. These effects are additive and translate to increased protein yield and piglet growth.

Probiotics are live micro-organisms that when administered in adequate amounts confer a health benefit on the host. Consumption of yoghurt has been shown to induce measurable health benefits linked to the presence of live bacteria. A number of human studies have clearly demonstrated that yoghurt containing viable bacteria (Streptococcus thermophilus and Lactobacillus delbrueckii sp. bulgaricus) improves lactose digestion and eliminates symptoms of lactose intolerance. Thus, these cultures clearly fulfil the current concept of probiotics.

We investigated the effect of different types of dietary protein on glycogen content in liver and skeletal muscle of exercise-trained rats. Twenty-four male Sprague-Dawley rats (approximately 100 g; n 6 per group) were divided into sedentary or exercise-trained groups with each group being fed either casein or whey protein as the source of dietary protein. Rats in the exercised groups were trained during 2 weeks using swimming exercise for 120 min/d, 6 d/week. Exercise training resulted in an increase in the skeletal muscle glycogen content. Furthermore, the whey protein group significantly increased the skeletal muscle glycogen content compared with the casein group. The increase in glycogen content in liver was significantly greater in rats fed the whey protein diet compared with those fed the casein diet. We also found that the whey protein diet increased the activity of liver glucokinase, whereas it decreased the activities of 6-phosphofructokinase and pyruvate kinase compared with the casein diet. However, hepatic total glycogen synthase activity and mRNA expression were similar with the two diets. In the skeletal muscle, whey protein decreased only 6-phosphofructokinase activity compared with casein. Total glycogen synthase activity in the skeletal muscle in the whey protein group was significantly higher than that in the casein group. The present study is the first to demonstrate that a diet based on whey protein may increase glycogen content in liver and skeletal muscle of exercise-trained rats. We also observed that whey protein regulated glycogen metabolism in these two tissues by different mechanisms.

Patients with Parkinson's disease (PD) often lose weight, but after subthalamic nucleus deep brain stimulation (STN-DBS), they gain weight. We compared daily energy intake (DEI), resting energy expenditure (REE) and substrate oxidation rates (measured by indirect calorimetry) in nineteen STN-DBS-treated patients (Group S), thirteen others on pharmacologic treatment by levodopa (Group L) and eight control subjects. We also determined the acute effects of STN-DBS and levodopa on REE and substrate oxidation rates. STN-DBS treated patients gained 9·7 (sem 7·1) kg after surgery, whereas patients on pharmacologic treatment lost 3·8 (sem 10·0) kg since diagnosis. In STN-DBS-treated patients, REE (−16·5 %; P<0·001), lipid oxidation (−27 %; P<0·05) and protein oxidation (−46 %; P<0·05) were decreased, whereas glucose oxidation was elevated (+81 %; P<0·05) as compared to patients on pharmacologic treatment. Levodopa acutely reduced REE (−8·3 %; P<0·05) and glucose oxidation (−37 %; P<0·01) with a slight hyperglycaemic effect (after levodopa challenge: 5·6 (sem 0·8) v. before levodopa challenge: 5·3 (sem 0·6) mmol/l; P<0·01). Switching ‘on’ STN-DBS acutely reduced REE (−17·5 %; P<0·01) and lipid oxidation (−24 %; P<0·001) 30 min after starting stimulation. Fasting glycaemia was slightly but significantly reduced (5·4 (sem 1·4) v. 5·5 (sem 1·3) mmol/l; P<0·01). After STN-DBS, the normalization of REE and the reduction in lipid and protein oxidation contribute to the restoration of weight. As levodopa decreases glucose oxidation, the reduction in daily dose of levodopa in STN-DBS-treated patients helps prevent the effect of weight gain on glycaemia.

Acute gut disorder is a cause for significant medicinal and economic concern. Certain individual pathogens of the gut, often transmitted in food or water, have the ability to cause severe discomfort. There is a need to manage such conditions more effectively. The route of reducing the risk of intestinal infections through diet remains largely unexplored. Antibiotics are effective at inhibiting pathogens; however, these should not be prescribed in the absence of disease and therefore cannot be used prophylactically. Moreover, their indiscriminate use has reduced effectiveness. Evidence has accumulated to suggestthat some of the health-promoting bacteria in the gut (probiotics) can elicit a multiplicity of inhibitory effects against pathogens. Hence, an increase in their numbers should prove effective at repressing pathogen colonisation if/when infectious agents enter the gut. As such, fortification of indigenous bifidobacteria/lactobacilli by using prebiotics should improve protection. There are a number of potential mechanisms for lactic acid bacteria to reduce intestinal infections. Firstly, metabolic endproducts such as acids excreted by these micro-organisms may lower the gut pH to levels below those at which pathogens are able to effectively compete. Also, many lactobacilli and bifidobacteria species are able to excrete natural antibiotics, which can have a broad spectrum of activity. Other mechanisms include an improved immune stimulation, competition for nutrients and blocking of pathogen adhesion sites in the gut. Many intestinal pathogens like type 1 fimbriated Escherichia coli, salmonellae and campylobacters utilise oligosaccharide receptor sites in the gut. Once established, they can then cause gastroenteritis through invasive and/or toxin forming properties. One extrapolation of the prebiotic concept is to simulate such receptor sites in the gut lumen. Hence, the pathogen is ‘decoyed’ into not binding at the host mucosal interface. The combined effects of prebiotics upon the lactic acid flora and anti-adhesive strategies may lead towards new dietary interventions against food safety agents.

Si-Jun-Zi decoction (SJZD), a traditional Chinese herbal prescription, has been used clinically for treating patients with disorders of the digestive system. Previous studies indicated that the polysaccharides of SJZD (SJZPS) are the active components contributing towards its pharmacological effects in improving gastrointestinal function and immunity. However, the protective and restitutive effects on intestinal epithelial cells remain unknown. In the present study, SJZPS were first extracted and chemically characterized. Then their stimulatory and restitutive effects on intestinal epithelial cells (IEC-6 cells) were elicited by different in vitro models including migration of wounded IEC-6 cells and cell proliferation. Results indicated that SJZPS not only protects the cells against the harmful impairment of indomethacin but also enhances re-epithelialization of a wounded monolayer at an optimal dose of 100 μg/ml at 24 h incubation. To elucidate the modulatory effect of SJZPS on wounded IEC-6 cells at the molecular level, an oligonucleotide microarray was employed to study differential gene expression of SJZPS-treated IEC-6 cells and the candidate genes were validated by RT-PCR. There was increased expression of genes coding for ion channels and transporters, which are critical to cell migration and restoration of wounded intestinal cells, suggesting a possible mechanism for re-epithelialization. In conclusion, our data show for the first time that SJZPS can enhance intestinal restitution and protect against indomethacin-induced damage of intestinal epithelial cells. These findings provide new insight into the mechanism of action of a traditional Chinese herbal prescription, SJZD, in intestinal wound restitution.

One of the debates in infant nutrition concerns whether dietary 18: 3n-3 (linolenic acid) can provide for the accretion of 22: 6 n-3 (docosahexaenoic acid, DHA) in neonatal tissues. The objective of the present study was to determine whether low or high 18: 3 n-3 v. preformed 22: 6 n-3 in the maternal diet enabled a similar 22: 6 n-3 content in the phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol (PI) and phosphatidylserine (PS) of glial cells from whole brain (cerebrum and cerebellum) of 2-week-old rat pups. At parturition, the dams were fed semi-purified diets containing either increasing amounts of 18: 3 n-3 (18: 2 n-6 to 18: 3 n-3 fatty acid ratio of 7·8: 1, 4·4: 1 or 1: 1), preformed DHA, or preformed 20: 4 n-6 (arachidonic acid)+DHA. During the first 2 weeks of life, the rat pups from the respective dams received only their dam's milk. The fatty acid composition of the pups' stomach contents (dam's milk) and phospholipids from glial cells were quantified. The 20: 4n-6 and 22: 6 n-3 content in the stomach from rat pups at 2 weeks of age reflected the fatty acid composition of the dam's diet. The 20: 4n-6 content of PE and PS in the glial cells was unaffected by maternal diet treatments. Preformed 22: 6 n-3 in the maternal diet increased the 22: 6 n-3 content of glial cell PE and PS compared with maternal diets providing an 18: 2n-6 to 18: 3 n-3 fatty acid ratio of 7·8: 1, 4·4: 1 or 1: 1 (P<0·0001). There was no significant difference in the 20: 4 n-6 and 22: 6 n-3 content of glial cell PC and PI among maternal diet treatments. It was concluded that maternal dietary 22: 6n-3 is more effective than low or high levels of maternal dietary 18: 3 n-3 at increasing the 22: 6 n-3 content in PE and PS of glial cells from the whole brain of rat pups at 2 weeks of age. The findings from the present study have important implications for human infants fed infant formulas that are devoid of 22: 6 n-3.

In pigs the extensive threonine utilization by the splanchnic tissues explains the relative inefficiency of dietary threonine conversion for body protein accretion. Two experiments were conducted to estimate the contribution of the portal drained viscera (PDV) and the liver to threonine metabolism and especially catabolism in growing pigs. In the first experiment, four pigs were surgically prepared for chronic catheter insertion in the portal, hepatic and jugular veins and in the carotid artery. They were continuously infused with l-[1-13C]threonine through the jugular catheter. The PDV and total splanchnic viscera (PDV and the liver) extracted 14·3 and 18·8 % of arterial threonine input, respectively. In a second experiment, we studied the metabolism of dietary threonine in the PDV and the liver in six female growing pigs. Animals were surgically prepared as in the first experiment except that l-[1-13C]threonine and [15N]glycine were continuously infused in the duodenum for 10 h. Unlabelled and labelled threonine and glycine PDV, liver and splanchnic tissues balance were calculated from plasma samples taken during the last 2 h of this infusion. Splanchnic tissues extracted 60 % of infused labelled threonine, 88 % of which was extracted by PDV so that threonine extraction by the liver was low. Both the liver and the pancreas can degrade threonine through the l-threonine 3-dehydrogenase pathway but not the intestine. Our data suggest that threonine catabolism through the l-threonine 3-dehydrogenase pathway was only a minor component of total threonine utilization in the splanchnic tissues.

The current epidemic of diabetes likely reflects marked changes in environmental factors, although genetic susceptibility plays a powerful role in the occurrence of diabetes in certain populations. We investigated whether long-term sucrose-drinking causes hyperglycaemia in male Wistar-Imamichi littermates (n 32), which are not genetically susceptible to diabetes or obesity. Each litter was divided equivalently into two groups, the sucrose group and the control group. The sucrose group received 300 g/l sucrose water and the control group received regular water until 42 weeks of age. Rats were weighed every 1 or 2 weeks. Oral glucose tolerance tests were performed at 28 and 36 weeks of age. Plasma glucose and insulin concentrations were measured. Body weights were significantly greater in the sucrose group than in the control group in 18-week-old rats (P<0·05), and the difference between the two groups reached 163 g by the end of the study (P<0·01). The 120 min post-load plasma glucose concentration in the sucrose group was 11·4 (sd 2·8) mmol/l in 28-week-old rats and 12·7 (sd 2·2) mmol/l in 36-week-old rats, while that of the control group remained approximately 7·3–7·7 mmol/l. In the sucrose group, the plasma insulin peak occurred 30 min post-load at 28 weeks of age; but the peak disappeared and hyperinsulinaemia was prolonged at 36 weeks of age. In conclusion, long-term sucrose-drinking causes increased body weight and glucose intolerance in normal male rats.

Although water is an important nutrient, there are no recommended intake values. Here, water intake, energy intake, physical activity and water loss was measured over 1 week in summer and in winter. Subjects were healthy volunteers, forty-two women and ten men, mean age of 29 (sd 7) years and mean BMI 21·8 (sd 2·2) kg/m2. Water intake was measured with a 7 d food and water record. Physical activity level (PAL) was observed as the ratio of total energy expenditure, as measured with doubly labelled water, to resting energy expenditure as measured in a respiration chamber. Water loss was measured with the deuterium elimination method. Water loss was highly reproducible and ranged from 0·20 to 0·35 l/MJ, independent of season and activity level, with higher values in women. Water loss was related to water and energy intake in summer (r 0·96, P<0·0001 and r 0·68, P<0·001, respectively) as well as in winter (r 0·98, P<0·0001 and r 0·63, P<0·01, respectively). Water loss was, for men, higher in subjects with a higher physical activity in summer (r 0·94, P<0·0001) and in winter (r 0·70, P<0·05). Normalizing water loss for differences in energy expenditure by expressing water loss in litres per MJ resulted in the same value for men in summer and winter. For women, physical activity-adjusted values of water loss were higher, especially in summer. In men, water turnover was determined by energy intake and physical activity, while seasonal effects appeared through energy expenditure. Women showed a higher water turnover that was unrelated to physical activity.

Lipid oxidation leads to meat spoilage and has been reported to cause adverse changes in the flavour and texture of poultry meat. Vitamin E has been found to be effective in delaying lipid oxidation. The aim of this study was to determine whether the vitamin E supplementation of chicken feed influences the consumers' perception of the quality of chicken meat under normal display and storage conditions. Untrained consumers (n 32) evaluated cooked breast meat from chickens (both corn fed and wheat fed) supplemented with 75 250 or 500 mg/kg vitamin E and after storage at 4°C for 4 and 7 d. Factorial analysis found an interaction between vitamin E treatment and storage day upon the perceived juiciness (P=0·023) and tenderness (P=0·041) of the chicken meat. Perceptions of quality relative to vitamin E level were more evident on day 4 than day 7. When the two cereal types were compared, the time-related sub-group effects were observed only in meat from corn-fed chickens supplemented with either 75 or 250 mg/kg, which was perceived to be juicier (P=0·018) and more tender (P=0·020) than that supplemented at the 500 mg/kg level. These results imply that the two lower concentrations of vitamin E have some advantages over 500 mg/kg, but for optimal consumer acceptance of corn-fed chicken meat, we suggest that 250 mg/kg vitamin E should be added to corn-fed poultry feed. There was no evidence to suggest any advantages in changing the current amount of vitamin E (75 mg/kg) used to rear wheat-fed birds.

Non-digestible inulin-type fructans, such as oligofructose and high-molecular-weight inulin, have been shown to have the ability to alter the intestinal microbiota composition in such a way that members of the microbial community, generally considered as health-promoting, are stimulated. Bifidobacteria and lactobacilli are the most frequently targeted organisms. Less information exists on effects of inulin-type fructans on the composition, metabolism and healthrelated significance of bacteria at or near the mucosa surface or in the mucus layer forming mucosa-associated biofilms. Using rats inoculated with a human faecal flora as an experimental model we have found that inulin-type fructans in the diet modulated the gut microbiota by stimulation of mucosa-associated bifidobacteria as well as by partial reduction of pathogenic Salmonella enterica subsp. enterica serovar Typhimurium and thereby benefit health. In addition to changes in mucosal biofilms, inulin-type fructans also induced changes in the colonic mucosa stimulating proliferation in the crypts, increasing the release of mucins, and altering the profile of mucin components in the goblet cells and epithelial mucus layer. These results indicate that inulin-type fructans may stabilise the gut mucosal barrier. Dietary supplementation with these prebiotics could offer a new approach to supporting the barrier function of the mucosa.