The changes in metabolic efficiency, body composition, and nutrient partitioning induced by high-fat feeding were evaluated in adult rats (90d of age). The alterations in serum free triiodothyronine, insulin, and leptin levels, as well as in hepatic and skeletal muscle metabolism, were also assessed. Rats were fed either a low- or a high-fat diet for 2 weeks. Relative to the low-fat feeding, energy intake and expenditure, as well as body-energy gain, lipid gain, and energetic efficiency, were increased by the high-fat feeding. Increased serum leptin levels accompanied these variations. A positive correlation between serum leptin levels and percentage of body fat was found in the rats fed the low- or high-fat diet, with a significant divergence between the slope of the regression lines. Furthermore, a negative correlation between serum leptin level and energy intake was found in the rats fed the low-fat diet, while a positive correlation was found in the rats fed the high-fat diet. Finally, the high-fat feeding decreased the hepatic and skeletal muscle mitochondrial oxidative capacity. It is concluded that, in adult rats, a nutritional factor such as a high level of fat in the diet induces obesity, leptin resistance, and impairment of mitochondrial capacity, all phenomena typical of unrestrained aged rats.

Retinyl palmitate added to Fe-fortified maize bread has been reported to enhance Fe absorption in adult Venezuelan subjects but not in Western Europeans. It is not known to what extent these results were influenced by differences in vitamin A status of the study subjects. The objective of the present study was to evaluate the influence of retinyl palmitate added to Fe-fortified maize porridge on erythrocyte incorporation of Fe in children with vitamin A deficiency, before and after vitamin A supplementation. Erythrocyte incorporation of Fe-stable isotopes was measured 14 d after intake of maize porridge (2·0 mg Fe added as ferrous sulfate) with and without added retinyl palmitate (3·5 μmol; 3300 IU). The study was repeated 3 weeks after vitamin A supplementation (intake of a single dose of 210 μmol retinyl palmitate; ‘vitamin A capsule’). Vitamin A status was evaluated by the modified relative dose–response (MRDR) technique. Retinyl palmitate added to the test meal reduced the geometric mean erythrocyte incorporation of Fe at baseline from 4·0 to 2·6 % (P=0·008, n 13; paired t test). At 3 weeks after vitamin A supplementation, geometric mean erythrocyte incorporation was 1·9 and 2·3 % respectively from the test meal with and without added retinyl palmitate (P=0·283). Mean dehydroretinol:retinol molar ratios were 0·156 and 0·125 before and after intake of the single dose of 210 μmol retinyl palmitate; ‘vitamin A capsule’ (P=0·15). In conclusion, retinyl palmitate added to the labelled test meals significantly decreased erythrocyte incorporation of Fe in children with vitamin A deficiency at baseline but had no statistically significant effect 3 weeks after vitamin A supplementation. The difference in response to retinyl palmitate added to Fe-fortified maize porridge on erythrocyte incorporation of Fe before and after intake of the vitamin A capsule indicates, indirectly, changes in vitamin A status not measurable by the MRDR technique. The lack of conclusive data on the effect of retinyl palmitate on Fe absorption indicates the complexity of the interactions between vitamin A status, dietary vitamin A and Fe metabolism.

The nutritional basis of breakdown of immunity to parasites may be addressed in a rodent model. We hypothesized that lactating rats would show a breakdown of immunity to Nippostrongylus brasiliensis, and that this breakdown of immunity would be sensitive to protein supply. Rats were immunized with 1600 infective N. brasiliensis larvae and subsequently mated. During lactation, these rats were offered foods with 90 (low protein; LP) or 210 (high protein, HP) g crude protein (N X 6.25)/kg and re-infected with 400, 800 or 1600 larvae on day 2 post-parturition. Immunized non-reproducing rats were offered a food containing 60 g crude protein/kg and re-infected with 1600 larvae. Seven days after secondary infection, lactating rats had more adult nematodes in their small intestine and nematode eggs in their colon contents than the non-reproducing rats. Protein supply did not affect worm or egg counts, although LP rats carried relatively more female nematodes than the HP rats. All lactating rats had lower intakes than expected from previous studies using similar nutritional protocols. This may have resulted in insufficient protein supply, even for the HP rats, and this could explain the absence of effects of protein supply on egg and worm counts. We conclude that a breakdown of immunity to N. brasiliensis can occur in lactating rats; this strongly suggests that the lactating rat is a suitable model for elucidating a possible nutritional basis of breakdown of immunity to parasites. However, sufficient protein intake must be achieved to address the hypothesis that breakdown of immunity to N. brasiliensis is sensitive to protein supply.

Butyrate is recognised as efficient in healing colonic inflammation, but cannot be used as a long-term treatment. Dietary fibre that produces a high-butyrate level when fermented represents a promising alternative. We hypothesised that different types of dietary fibre do not have the same efficiency of healing and that this could be correlated to their fermentation characteristics. We compared short-chain fructo-oligosaccharides (FOS) and type 3 resistant starch (RS) in a previously described dextran sulfate sodium (DSS)-induced colitis model. Seventy-two Sprague–Dawley rats received water (control rats) or DSS (50g DSS/l for 7d then 30g DSS/l for 7 (day 7) or 14 (day 14) d). The rats were fed a basal diet (BD), or a FOS or RS diet creating six groups: BD-control, BD-DSS, FOS-control, FOS-DSS, RS-control and RS-DSS. Caeco-colonic inflammatory injuries were assessed macroscopically and histologically. Short-chain fatty acids (SCFA) were quantified in caeco-colon, portal vein and abdominal aorta. At days 7 and 14, caecal and distal macroscopic and histological observations were improved in RS-DSS compared with BD-DSS and also with FOS-DSS rats. Caeco-colonic SCFA were reduced in FOS-DSS and RS-DSS groups compared with healthy controls. The amount of butyrate was higher in the caecum of the RS-DSS rats than in the BD-DSS and FOS-DSS rats, whereas distal butyrate was higher in FOS-DSS rats. Partially explained by higher luminal levels of SCFA, especially butyrate, the healing effect of RS confirms the involvement of some types of dietary fibre in inflammatory bowel disease. Moreover, the ineffectiveness of FOS underlines the importance of the type of dietary substrate.

Ascorbic acid and Na2EDTA enhance Fe absorption from the water-soluble Fe compound FeSO4 but their effect on poorly water-soluble Fe compounds such as ferrous fumarate is less well established. In the present study, the effects of ascorbic acid and Na2EDTA on Fe absorption from ferrous fumarate were evaluated in adult women (ten women/study) from the erythrocyte incorporation of Fe stable isotopes (57Fe or 58Fe) 14 d after administration. Two separate studies were made with test meals of Fe-fortified infant cereal (5 mg Fe/meal). Data were evaluated by paired t tests and the results are presented as geometric means. In study 1a, the comparison between Fe absorption from ferrous fumarate- and FeSO4-fortified cereal showed that adult women absorb Fe as well from ferrous fumarate as from FeSO4 (3·0 and 3·1 % respectively, P=0·85). After addition of Na2EDTA (Na2EDTA:fortification Fe molar ratio of 1:1), Fe absorption from FeSO4 was significantly higher than from ferrous fumarate (5·3 v. 3·3 % respectively, P<0·01; study 1b). In study 2, Fe absorption was compared from ferrous fumarate-fortified meals with and without ascorbic acid added at a 4:1 molar ratio (relative to fortification Fe) and the results showed that ascorbic acid increased Fe absorption from ferrous fumarate significantly (6·3 v. 10·4 %, P=0·02). The results of the present studies show that Fe absorption from ferrous fumarate is enhanced by ascorbic acid but not by Na2EDTA, thus emphasising that not all findings from Fe absorption studies made with FeSO4 can be extrapolated to Fe compounds with different solubility properties.

As the physiological roles of dietary lecithin have not yet been clearly defined, we examined the effects of lecithin on lipid absorption in male Wistar rats with a mesenteric lymph cannula. Lymphatic absorption was observed after the infusion of 1 ml emulsion containing 100 mg test oil emulsified with sodium taurocholate (10 g/l) in three separate experiments. Test oils (100 mg) were: soyabean oil (triacylglycerol (TG) source, SO) and soyabean oil + lecithin (75 mg soyabean oil+25 mg lecithin, LE) in Expt 1; SO, LE or soyabean oil + lysolecithin (75 mg soyabean oil plus 25 mg lysolecithin, LY) in Expt 2; hydrolysed soyabean oil (HSO) or HSO+lysolecithin (75 mg HSO+25 mg lysolecithin, HLY) in Expt 3. After LE and LY infusions, lymph flow and the lymphatic output of TG was higher than after SO infusion at 0-30 min and 0-90 min respectively (Expts 1 and 2). Lecithin-induced increases in lymph TG output remained constant when HSO was infused (Expt 3). There were no differences in the TG:phospholipid ratio in the lymph after infusion among the groups; nevertheless, the lymphatic output of TG was much higher after infusion with LE than with SO. Fatty acid was released more efficiently from SO than from LE and LY by in vitro digestion with rat bile–pancreatic juice. These present results demonstrate that a TG emulsion containing soyabean lecithin or its hydrolysates promote lymphatic TG output and suggest that the increases in TG absorption do not depend on TG digestion.

Several flavonoids have shown their anti-carcinogenic effects in various models. The soyabean isoflavone genistein was demonstrated earlier in our laboratory to be an effective inhibitor of dimethylbenz[a]anthracene (DMBA)-induced DNA damage in MCF-7 cells by curbing cytochrome P450 (CYP) 1 enzymes. The red clover (Trifolium pratense) isoflavone biochanin A is a methylated derivative of genistein, and its anti-mutagenic effect in bacterial cells has been shown previously. Because of its protection against chemical carcinogenesis in an animal model, biochanin A was selected for testing in our established MCF-7 cell system. From the results obtained in the semi-quantitative reverse transcription–polymerase chain reaction and xenobiotic response element (XRE)–luciferase reporter assays, biochanin A could reduce xenobiotic-induced CYP1A1 and -1B1 mRNA abundances through the interference of XRE-dependent transactivation. Enzyme kinetic studies also indicated that biochanin A inhibited both CYP1A1 and -1B1 enzymes with inhibition constant (Ki) values 4·00 and 0·59μM respectively. Since the biotransformation of DMBA was dependent on CYP1 enzyme activities, biochanin A was able to decrease the DMBA–DNA lesions. The present study illustrated that the red clover isoflavone could protect against polycylic aromatic hydrocarbon-induced DNA damage.

Reduced protein intake during pregnancy decreased maternal hepatic and plasma docosahexaenoic acid concentrations and impaired docosahexaenoic acid accumulation into fetal brain in the rat. The present study investigated whether restriction of maternal protein intake during pregnancy in the rat alters membrane phospholipid fatty acid composition in the offspring after weaning. Female rats (six per group) were mated and fed diets containing either 180 or 90 g protein/kg throughout pregnancy. Mothers were transferred to standard chow after delivery and the litters reduced to eight pups. Weaning was at 28 d and pups were killed 5 to 6 d later. Tissue weights or membrane total phosphatidylcholine (PC) and phosphatidylethanolamine (PE) concentrations in the offspring did not differ between dietary groups. There were significant differences between the 180 and 90 g/kg groups in liver, brain, lung and heart fatty acid composition that differed between tissues and phospholipid classes. For example, docosahexaenoic and arachidonic acid concentrations were 23 and 10 % lower respectively in hepatic PC, but not PE, in the 90 g/kg group. In brain, docosahexaenoic acid concentration was 17 % lower in PC, but not PE, while arachidonic acid content was 21 % greater in PE but unchanged in PC. The greatest differences were in unsaturated fatty acids, which suggests alterations to desaturase activities and/or the specificity of phospholipid biosynthesis. These results suggest that restricted maternal protein intake during pregnancy results in persistent alterations to membrane fatty acid content.

Dietary studies are often conducted as longitudinal intervention or crossover trials using multiple days of measurement on each subject during each of several measurement periods, and determining the required numbers of days and subjects is important in designing these studies. Linear mixed statistical models were used to derive equations for precision, statistical power and sample size (number of days and number of subjects) and to obtain estimates of between-subject, period-to-period, and day-to-day variation needed to apply the equations. Two cohorts of an on-going exercise intervention study, and a crossover study of Olestra, each with 14 d of measurement/subject per period, were used to obtain estimates of variability for energy and macronutrient intake. Numerical examples illustrate how the equations for calculating the number of days or number of subjects are applied in typical situations, and sample SAS code is given. It was found that between-subject, period-to-period, and day-to-day variation all contributed significantly to the variation in energy and macronutrient intake. The ratio of period-to-period and day-to-day standard deviations controls the trade-off between the number of days and the number of subjects, and this remained relatively stable across studies and energy and macronutrient intake variables. The greatest gains in precision were seen over the first few measurement days. Greater precision and fewer required days were noted in the study (Olestra) that exerted greater control over the subjects and diets during the feeding protocol.

Many adult diseases, including type 2 diabetes, hypertension and cardiovascular disease, are related to low birth weight. The mechanistic basis of this relationship is not known. To investigate the role of fetal undernutrition, we used a rat model of maternal protein restriction in which dams were fed a diet containing 80 g protein/kg (v. 200 g/kg in the control group) throughout gestation and lactation. Offspring were born smaller than controls and in adulthood developed diabetes, hyperinsulinaemia and tissue insulin resistance. To determine possible mechanisms of fetal programming, circulating levels of several hormones were measured in maternal plasma at gestational days 14, 17 and 21 and fetal plasma at gestational day 21. Several differences were noted at day 14, when glucose concentrations in maternal and feto–placental blood were raised significantly (P=0·04 and P=0·0001 respectively); insulin levels in the low-protein (LP) dams were raised (P=0·04), prolactin levels were raised (P=0·047) and progesterone levels were reduced (P=0·02). Circulating 17β-oestradiol in the LP dams was raised by 35% over those of the controls from day 17 to day 21 (P=0·008). A significant decrease in maternal leptin levels (P=0·004) was observed at gestation on day 21. Neither oestradiol nor leptin levels were altered in the fetal circulation at day 21. Maternal and fetal corticosterone levels were comparable with control levels, suggesting that they do not initiate the programming effects in this model. Our present results suggest that maternal protein restriction imposes changes in maternal levels of glucose, insulin, prolactin, progesterone, oestradiol and leptin; these changes could influence the programming of eventual adult disease in the developing fetus.

According to the report of the World Health Organization (1985), total energy expenditure (TEE) in human subjects can be calculated as BMR×physical activity level (PAL). However, other reports have pointed out limitations in the suggested procedure related to the % body fat of the subjects. The purpose of the present study was to evaluate the World Health Organization (1985) procedure in thirty-four healthy women with BMI 18–39kg/m2. BMR and TEE were measured using indirect calorimetry (BMRmeas) and the doubly-labelled water method (TEEref) respectively. When assessed using the doubly-labelled water and skinfold-thickness methods, the women had 34 (sd 8) and 33 (sd 6) % body fat respectively. On the basis of guidelines provided by the World Health Organization (1985), 1·64 was selected to represent the average PAL of the women. Furthermore, PAL was also assessed by means of an accelerometer (PALacc), heart-rate recordings (PALHR) and a questionnaire (PALq). These estimates were: PALacc 1·71 (sd 0·17), PALHR 1·76 (sd 0·24), PALq 1·86 (sd 0·27). These values were lower than TEEref/BMRref, which was 1·98 (sd 0·21). BMR assessed using equations recommended by the World Health Organization (1985) (BMRpredicted) overestimated BMR by 594 (sd 431) kJ/24h. However, when TEE was calculated as BMRpredicted×PALacc, BMRpredicted×PALHR and BMRpredicted×PALq respectively, average results were in agreement with TEEref. Furthermore, TEE values based on BMRpredicted and PALacc, PALHR, PALq as well as on PAL=1·64, minus TEEref, were significantly correlated with body fatness. When the same PAL value (1·64) was used for all subjects, this correlation was particularly strong. Thus, the World Health Organization (1985) procedure may give TEE results that are biased with respect to the body fatness of subjects.

Long-Evans Cinnamon (LEC) rats spontaneously develop fulminant hepatitis, associated with excess Cu accumulation in the liver: thus, they are considered an animal model of Wilson's disease. In the present study, we investigated the ability of excess dietary histidine to reduce the excess accumulation of liver Cu in LEC rats by comparing them with Fischer rats. The results clearly showed that the excess-histidine diet markedly stimulated the Cu excretion in urine, and significantly decreased the liver Cu content in LEC rats by 47·5%. The serum Cu content in LEC rats was not influenced by excess dietary histidine. We also compared the effects of excess dietary histidine on some liver antioxidant enzyme activities, liver and serum lipid levels and serum alanine aminotransferase activity of LEC and Fischer rats. Dietary histidine decreased the activities of total and Cu, Zn-superoxide dismutase in the liver of both strains. In LEC rats, the liver cholesterol content decreased, and serum cholesterol and phospholipids levels increased on feeding the excess-histidine diet. When fed on the basal diet, the serum alanine aminotransferase activity was higher in LEC rats than in Fischer rats, but a significant decrease in serum alanine aminotransferase activity of LEC rats was observed on feeding the excess-histidine diet. These results suggest that excess dietary histidine is effective in removing Cu ions from the liver of LEC rats. Thus, it may be of benefit in the prevention or treatment of liver injury in LEC rats and in patients with Wilson's disease.

Fructo-oligosaccharides (FOS) may have potential benefits, since they exhibit many soluble dietary fibre-like properties. Foods currently available for weaning infants are generally low in fibre content and lack these potential benefits. Data documenting tolerance of FOS in weaning foods are greatly lacking. Our present objective was to evaluate the tolerance and gastrointestinal effects of FOS-supplemented infant cereal used as a daily addition to the diet of healthy infants. Healthy infants were randomly assigned to receive either 0·75 g FOS per serving of cereal or placebo for 28 d. The primary outcome of interest was gastrointestinal tolerance, which was assessed by daily parental reporting of functional variables for 28 d, including stool patterns and signs and symptoms of gastrointestinal tolerance. Secondary outcomes were also measured including: cereal intake (g cereal and g FOS/d), stool pH, changes in anthropometric measurements and adverse events. The study population included a total of fifty-six infants, age range 16·2–46·2 weeks with a mean age of 32·5 (sd 8·9) weeks; twenty-nine infants were randomized to the control group (age 31·8 (sd 9·0) weeks) and twenty-seven to the FOS-supplemented group (34·7 (sd 8·9) weeks). Average daily total intake per infant and average intake per serving were similar in both groups. Average FOS consumption was 0·74 (sd 0·39) g/d and as high as 3·00 g/d. Stool consistency was less likely to be described as ‘hard’, and more likely to be described as ‘soft’ or ‘loose’, in the FOS v. control group. The mean number of stools per infant was 1·99 (sd 0·62) per d in the FOS-supplemented group compared with 1·58 (sd 0·66) in the control group (P=0·02). There were no differences between the groups in reporting for crying, spitting-up or colic. No differences were found for stool pH. FOS-supplements added to cereal were well tolerated in doses of up to 3·00 g/d. FOS consumption led to more regular and softer stools, without diarrhoea, as well as less-reported frequency of symptoms associated with constipation such as hard stools or skipped days without stool. The present study is one of few studies documenting tolerance to increased fibre intake in the form of FOS as part of a weaning food.

Postprandial glycaemic control is important in the prevention and therapy of type 2 diabetes and related diseases. Agents that may reduce postprandial glycaemia and/or insulinaemia, such as consumption of high-amylose foods, are considered beneficial; however, little is known about the dose–response relationship and the effects of cooking. The aim of the present study was to define the dose–response curve for postprandial glycaemic and insulinaemic excursions following meals of different amylose content and to compare the dose–response curves for meals containing cooked and uncooked starches. Following an overnight fast, rats ingested a test meal and blood was sampled over 2 h. The meal was given at 1.0 g carbohydrate/kg body weight, with an amylose content of 0, 270, 600 or 850 g/kg total starch. The area under the glucose curve did not differ under any condition investigated. For the uncooked-starch diets, area under the insulin curve was higher for the 0 g amylose/kg total starch meal than all other meals (P = 0·0001). For the cooked-starch diets, area under the insulin curve was higher in the O than the 600 and 850 g amylose/kg total starch groups (P < 0·01), but did not differ from the 270 amylose/kg total starch group. These results suggest that even a relatively small proportion of uncooked amylose (270 g/kg total starch) is sufficient to achieve a maximal attenuating effect on postprandial insulin concentrations as compared with 0 g amylose/kg total starch. Following cooking, however, a much higher proportion of amylose (≥ 600 g/kg total starch) is needed to achieve a similar effect.

The main objectives of the present study were to determine the effect of dietary conjugated linoleic acid (CLA) isomers on the fatty acid composition and cholesterol content of egg-yolk lipids. Forty-five 25-week-old laying hens were randomly distributed into five groups of nine hens each and maintained in individual laying cages, throughout 12 weeks of the experiment. They were assigned to the five treatments that consisted of commercial layer diets containing 0, 5, 10, 15 or 20g pure CLA/kg. Feed intake of hens varied little and insignificantly. Egg mass was uniformly lower (P<0·05) in the hens fed the CLA-enriched diets. Feed conversion efficiency, when expressed per kg eggs, was impaired (P<0·05), although without obvious relation to the dietary CLA concentration. Feeding the CLA-enriched diets resulted in gradually increasing deposition of CLA isomers (P<0·01) in egg-yolk lipids. Saturated fatty acids were increased (P<0·01) and monounsaturated fatty acids decreased (P<0·01). Polyunsaturated fatty acids (PUFA), when expressed as non-CLA PUFA, were also significantly decreased (P<0·01). The most striking effects (P<0·01) were observed for palmitic (16 : 0) and stearic (18 : 0) acids, which increased from 23·6 to 34% and from 7·8 to 18%, respectively. On the other hand, oleic acid (18 : 1n-9) decreased from 45·8 to 24·3%. Among non-CLA PUFA, linoleic (18 : 2n-6) and α-linolenic (18 : 3n-3) acids were strongly (P<0·01) decreased, from 14·2 to 7·7% and from 1·3 to 0·3%, respectively. The same was true for arachidonic (20:4n-6) and docosahexaenoic (22 : 6n-3) acids. The cholesterol content of egg yolks, when expressed in mg/g yolk, was not affected by the dietary CLA concentrations. In conclusion, unless the adverse effects of CLA feeding to laying hens on the fatty acid profile of egg yolks are eliminated, the CLA-enriched eggs cannot be considered functional food products.

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

The present investigation was undertaken to evaluate whether mitochondrial energy metabolism is altered in a model of malnutrition induced by dexamethasone (DEX) treatment (1·5mg/kg per d for 5d). The gastrocnemius and liver mitochondria were isolated from DEX-treated, pair-fed (PF) and control (CON) rats. Body weight was reduced significantly more in the DEX-treated group (−16%) than in the PF group (−9%). DEX treatment increased liver mass (+59% v. PF, +23% v. CON) and decreased gastrocnemius mass. Moreover, in DEX-treated rats, liver mitochondria had an increased rate of non-phosphorylative O2 consumption with all substrates (approximately +42%). There was no difference in enzymatic complex activities in liver mitochondria between rat groups. Collectively, these results suggest an increased proton leak and/or redox slipping in the liver mitochondria of DEX-treated rats. In addition, DEX decreased the thermodynamic coupling and efficiency of oxidative phosphorylation. We therefore suggest that this increase in the proton leak and/or redox slip in the liver is responsible for the decrease in the thermodynamic efficiency of energy conversion. In contrast, none of the variables of energy metabolism determined in gastrocnemius mitochondria was altered by DEX treatment. Therefore, it appears that DEX specifically affects mitochondrial energy metabolism in the liver.

The aim of the present study was to explore the nature, extent and probable causes of nutritional deficiencies among children with disabilities living in Dharavi, a slum in Mumbai, India. A cross-sectional study was conducted to investigate whether the nutritional status of children with disabilities, aged 2–6 years (n 141), was worse than that of non-disabled sibling controls (n 122) and neighbour controls (n 162). Data on food patterns, anthropometry, micronutrient status and feeding difficulties reported by parents were collected. The mean weight for age of the children with disabilities (−2·44 (sd 1·39) Z scores; n 120) was significantly lower (P<0·05) compared with the sibling (−1·70 (sd 1·20) Z scores; n 109) and neighbour (−1·83 (sd 1·290) Z scores; n 162) control groups. The children with disabilities had significantly lower (P<0·05) mean haemoglobin levels (92 (sd 23) g/l; n 134) compared with siblings (102 (sd 18) g/l; n 103) and neighbours (99 (sd 18) g/l; n 153). Relative risk (RR) analysis indicated that the disabled children with feeding difficulties were significantly more likely (P<0·05) to be malnourished, by the indicator of weight for age (RR 1·1; 95 % CI 1·08, 1·20) compared with the disabled children without a feeding difficulty. They were also significantly more likely to be malnourished using the indicators of height for age (RR 1·3; 95 % CI 1·19, 1·43) and weight for height (RR 2·4; 95 % CI 1·78, 3·23) compared with the disabled children without a feeding difficulty. Feeding difficulties were identified as a risk factor for vulnerability to inadequate nutritional status among children with disabilities.

Single 13C6-labelled doses of pteroylmonoglutamic acid (PteGlu; 634 nmol) or 5-formyltetrahydrofolic acid (431–569 nmol) were given to fasted adult volunteers, and the rise in total and 13C-labelled plasma 5-methyltetrahydrofolic acid metabolite monitored over 8 h by HPLC and liquid chromatography–MS. The dose-adjusted area under the curve (AUC) for total (labelled plus unlabelled) plasma 5-methyltetrahydrofolic acid following a 5-formyltetrahydrofolic acid test dose was 155 % that obtained following a PteGlu test dose. Surprisingly, an average 60 and 40 % of the total plasma 5-methyltetrahydrofolic acid response to [13C6]PteGlu and [13C6]5-formyltetrahydrofolic acid, respectively, was unlabelled; an observation never before reported. Short-term kinetics of plasma [13C6]5-methyltetrahydrofolic acid showed a slower initial rate of increase in plasma concentration and longer time to peak following an oral dose of [13C6]PteGlu compared with that for an oral dose of [13C6]5-formyltetrahydrofolic acid, while the [13C6]5-methyltetrahydrofolic acid AUC for [13C6]5-formyltetrahydrofolic acid was 221 % that for [13C6]PteGlu. These data indicate that PteGlu and 5-formyltetrahydrofolic acid, which are thought to be well absorbed (about 90 %) at physiological doses, exhibit dramatically different rates and patterns of plasma response. A limitation in the rate of reduction of PteGlu before methylation could result in slower mucosal transfer of [13C6]5-methyltetrahydrofolic acid derived from [13C6]PteGlu into the plasma. This, when coupled with an observed similar plasma clearance rate for [13C6]5-methyltetrahydrofolic acid metabolite derived from either folate test dose, would yield a comparatively smaller AUC. These findings suggest potential problems in interpretation of absorption studies using unlabelled or labelled folates where the rate of increase, the maximum increase, or the AUC, of plasma folate is employed for test foods (mainly reduced folates) v. a ‘reference dose’ of PteGlu.

Upon admission to hospital, 30–50% of patients either are or become malnourished. There is no generally accepted definition of malnutrition or guidelines on the best way to establish nutritional status. We consider it self-evident that the nursing staff have an important role in screening patients at risk of malnutrition on admission and thereafter at regular times. This is why we developed the nursing nutritional screening form (NNSF). The NNSF was tested by nurses, dietitians and clinicians, in pairs, to establish the extent of agreement in two phases on sixty-nine and forty patients. Later, the form was used in practice by nursing staff on five wards (334 patients). Based on the results of the NNSF, patients were referred to a dietitian. The dietitian established whether the patient was indeed at risk, or was actually malnourished, using a complete nutritional history. The degree of concurrence within pairs was reasonable to good. The same applied to the concurrence between nursing staff and dietitians, but concurrence between clinicians and nursing staff was less. In total, 334 patients were screened and sixty-nine of them were referred to the dietitian. It was established that 86% of the referred patients were potentially at risk of malnutrition or were malnourished. Without the NNSF, 39% (n 27) of the patients referred to the dietitian would not have been referred, or would have been referred much later. The NNSF makes it possible for nurses to detect malnourished patients or patients at risk of malnutrition at an early stage of their hospitalization.