An inhibitor of α-amylase was isolated and purified from an extract of white kidney beans (Phaseolus vulgaris). The acute oral administration of the inhibitor (50 mg/kg body weight) to adult Wistar rats together with a starch load (2 g/kg body weight suspended in NaCl (9 g/l)) reduced the increase in glycaemia over the basal value (NaCl, 222 (SEM 49); inhibitor, 145 (SEM 16) mmol/l×180 min; P<0.05) without modifying the insulin response. On administering the inhibitor orally (50 mg/kg body weight dissolved in NaCl (9 g/l)) for 21 d to rats fed on a standard diet, a decline was observed in the glycaemia values on day 0 (NaCl, 5.53 (SEM 0.12); inhibitor, 5.25 (SEM 0.16) mmol/l) relative to those obtained on days 10 (NaCl, 5.00 (SEM 0.14); inhibitor, 4.60 (SEM 0.08) mmol/l; P<0.05) and 21 (NaCl, 5.22 (SEM 0.22); inhibitor, 4.50 (SEM 0.12) mmol/l; P<0.01) of treatment, without modifying the plasma concentration of insulin. There was found to be a significant anorexigenic action of the inhibitor; there was reduced food intake (NaCl, 23.07 (SEM 0.31); inhibitor, 19.50 (SEM 0.49) g/d; P<0.01), a reduced weight gain (NaCl, 52 (SEM 3); inhibitor, −1.33 (SEM 8.9) g/21 d; P<0.01), as well as changes in the activity of some intestinal enzymes such as maltase (NaCl, 87 (SEM 7); inhibitor, 127 (SEM 11) U/g proteins; P<0.05). The present study has shown, for the first time, that the prolonged administration of an α-amylase inhibitor reduces blood glucose levels and body-weight gain in Wistar rats.

Three xylanase products, xylanase A derived from Thermomyces lanuginosus, xylanase B from Humicola insolens and xylanase C from Aspergillus aculeatus, were examined for their effects on the nutritive value of wheat. The study investigated the effects of enzyme addition to broiler diets based on a low-metabolisable-energy (ME) wheat and a normal-ME wheat, with the emphasis on changes in composition of the NSP along the digestive tract in broiler chickens. There were significant (P>0·01) enzyme and wheat effects on the apparent ME, but there was no wheat×enzyme interaction on apparent ME. Weight gain and feed conversion efficiency (except xylanase C for normal wheat) were also significantly (P>0·01) increased by the xylanases. The enzymes differed in their effect on a number of important nutritional parameters. Xylanase A reduced (P>0·05) the excreta moisture level from 77·1% in birds fed the normal-ME wheat control to 73·4% and from 77·4% in those fed the low-ME wheat to 73·0%. The other two enzymes did not affect excreta moisture levels. The digesta viscosity in the duodenum, jejunum and ileum of birds fed both types of wheat was reduced (P>0·01) by xylanases A and C, but was increased (P>0·01) in the jejunum and ileum by xylanase B. The digestibility of the soluble NSP was mostly negative in the small intestine. The digestibility of the insoluble NSP differed (P>0·01) between the two wheats, with those in the low-ME wheat being more digestible (14 v. 28%). When supplemented with xylanase A, the ileal digestibility of the insoluble NSP in the normal- and low-ME wheats was increased by 28 and 42?%, respectively. Xylanases B and C did not affect the digestibility of the insoluble NSP regardless of wheat type. It may be concluded that wheats with low or normal ME values vary in their responses to xylanase supplementation. Apart from having an elevated level of soluble NSP, low-ME wheat may also contain insoluble NSP, which in the present study appeared to be more easily degradable in the gut of the chicken.

We studied the effects of five high-fat semi-purified diets varying at a 4 % (w/w) level in either stearic, oleic, linoleic, α-linolenic, or γ-linolenic acid on body fat and energy metabolism in BALB/c mice. A diet containing caprylic, capric, lauric, and myristic acid was used as a reference diet and a diet with 4 % conjugated linoleic acid (CLA) was used as a positive control as it is known to effectively lower body fat in mice. The diets were fed for 35 d. Body fat was significantly lower in the CLA group than in the other groups but was not significantly different among the non-CLA groups. Among the non-CLA groups, the linoleic acid group tended to have the highest and the α-linolenic acid group the lowest proportion of body fat. In energy-balance studies, the percentage of energy intake that was stored in the body was significantly lower in the CLA group compared with the other dietary groups. The percentage of energy intake eliminated in excreta was highest in the stearic acid group followed by the γ-linolenic acid group. These results were reflected in apparent fat digestibility, which was lowest in the stearic acid group. The percentage of energy intake expended as heat was highest in the CLA-fed mice. The results of the present study suggest that body fat and energy accretion in mice fed diets containing different C18 fatty acids is by far the lowest with CLA and that linoleic acid produced the highest fat intake and energy accretion.

We examined the alterations in vitamin A metabolism as a result of flupenthixol or cefotiam administration. The impact of these drugs on indices of vitamin A status was evaluated in Brown Norway and Long–Evans rats. Intramuscular drug administration for 28 d resulted in a decline in systemic retinol. Changes in circulating retinol with time for chronic dosing showed drug treatment (P<0·001) and time (P<0·03) to be significant factors, but rat strain (P=0·33) was not a significant factor. Flupenthixol was the most active retinol-lowering compound (P<0·005). At the end of the 28 d period, hepatic retinyl ester hydrolase activity was greater in drug-treated rats than in controls (P<0·05). With regard to effects on liver reserves: (1) flupenthixol treatment resulted in vitamin A depletion (P<0·05); (2) cefotiam treatment stimulated vitamin A accumulation; (3) distinctive patterns of retinol and its esters were seen in response to treatment. It is reasonable to assume that the drugs interfere with vitamin A in at least two ways: (1) lowering of plasma retinol, an early event in the interaction, may be caused by inhibition of hepatic holo-retinol-binding protein secretion or stimulation of clearance, or both; (2) when plasma retinol levels are persistently low, and as the hepatic deposits of the xenobiotics build up, there are changes in the vitamin A pool size and composition of the liver. Candidate enzymes are retinyl ester hydrolase and cytochrome P450. The relationship between these two events will be studied in further detail.

Traditionally hand-pressed argan oil, obtained from Argania spinosa seeds, is eaten raw in south-west Morocco; its rich composition of tocopherols, MUFA and PUFA make a study of its actions on risk factors for CVD, such as hypertension, interesting. The effects of 7 weeks of treatment with argan oil (10ml/kg) on the blood pressure and endothelial function of spontaneously hypertensive rats (SHR) and normotensive Wistar–Kyoto rats were investigated. Systolic blood pressure and heart rate were measured every week by the tail-cuff method and endothelial function was assessed by carbachol (10−8 to 10−4m)-induced relaxations of aortic rings and small mesenteric arteries pre-contracted with phenylephrine. Argan-oil administration reduced the mean blood pressure of SHR after the fifth week of treatment (P<0·05) and increased (P<0·01) the endothelial responses of arteries from SHR. The NO synthase inhibitor, l-N-ω-nitroarginine (3×10−5m) revealed a greater participation of NO in the relaxant effect after the treatment. When cyclooxygenase (COX) was blocked with indomethacin (10−5m), an involvement of COX products in the endothelium-dependent response was characterized. Enzyme immunoassay of thromboxane B2 showed a significant decrease (P<0·05) in the release of thromboxane A2 in both aorta and small mesenteric artery after argan-oil treatment of SHR. Experiments in the presence of the thromboxane A2–prostaglandin H2 receptor antagonist ICI 192, 605 (10−5m) confirmed this result. Results after incubation with the antioxidants superoxide dismutase and catalase suggested that a decreased oxidative stress might contribute to explain the beneficial effects of argan-oil treatment.

The aim of the present study was to compare the protein-free diet, guanidinated casein (GuC) and enzyme hydrolysed casein (EHC) methods for the quantification of endogenous amino acid (AA) flow in the avian ileum. Growing broiler chickens (5 weeks old) were used. All three assay diets were based on dextrose, and in the GuC and EHC diets GuC or EHC were the sole source of N. Endogenous AA flows determined with the use of protein-free diet were considerably lower (P>0·05) than those determined by the GuC and EHC methods. The total endogenous AA flows determined by the GuC and EHC methods were almost 3-fold greater (P>0·05) than those determined by the protein-free diet. The endogenous AA values obtained from GuC and EHC methods were similar (P<0·05), except for the flow of arginine, which was lower (P>0·05) in the EHC method. Glutamic acid, aspartic acid, threonine and glycine were the predominant endogenous AA present in digesta from the distal ileum. The contents of methionine, histidine and cystine were lower compared with other AA. The method of determination had no effect on the AA composition of endogenous protein, except for threonine, glutamic acid, lysine, arginine and cystine. The concentrations of threonine and arginine were lower (P>0·05) and that of lysine was higher (P>0·05) with the EHC method compared with the other two methods. The concentration of glutamic acid was greater (P0·05) and that of cystine was lower (P>0·05) in the EHC and GuC methods compared with the protein-free diet method. The results showed that the ileal endogenous flows of N and AA are markedly enhanced by the presence of protein and peptides, above those determined following feeding of a protein-free diet. It is concluded that the use of EHC and GuC methods enables the measurement of ileal endogenous losses in chickens under normal physiological conditions.

The knowledge base underpinning the setting of nutrient requirements for children and adolescents is not very secure. The advent of the concepts of optimal nutrition and functional foods has encouraged the possible use of functional effects as criteria for adequate nutrition in this age group. Target functions have been identified for growth development and differentiation and for behavioural and cognitive development. However, ideal markers or effects for these are not generally available. Additionally, nutrition in young people should avoid predisposing them to diet-related disease in later life. It is suggested that functional effects should include markers of reduction of risks of disease (nutritional safety) as well of benefits for health and well-being. Such markers of functional effects should be expected to arise from fundamental studies of nutrient–gene interactions and post-genomic metabolism.

The influence of protein and amino acid on the control of food intake and the specific control of protein and amino acid intakes remains incompletely understood. The most commonly accepted conclusions are: (1) the existence of an aversive response to diets deficient in or devoid of protein or deficient in at least one essential amino acid; (2) the existence of a mechanism that enables attainment of the minimum requirement for N and essential amino acids by increasing intake of a low-protein diet; (3) a decrease in the intake of a high-protein diet is associated with different processes, including the high satiating effect of protein. Ingested proteins are believed to generate pre- and post-absorptive signals that contribute to the control of gastric kinetics, pancreatic secretion and food intake. At the brain level, two major afferent pathways are involved in protein and amino acid monitoring: the indirect neuro-mediated (mainly vagus-mediated) pathway and the direct blood pathway. The neuro-mediated pathway transfers pre-absorptive and visceral information. This information is for the main part transferred through the vagus nerve that innervates part of the oro-sensory zone: the stomach, the duodenum and the liver. Other information is directly monitored in the blood. It is likely that the system responds precisely when protein and essential amino acid intake is inadequate, but in contrast allows a large range of adaptive capacities through amino acid degradation and substrate interconversion.

The effects of alcohol on food and energy intake in human subjects have been the subject of a number of controlled studies recently. Unlike the evidence for other macronutrients, there is minimal evidence for any compensatory reduction in food intake in response to energy ingested as alcohol. In contrast, all studies testing intake within 1 h of preload ingestion report a higher intake of food following alcohol relative to energy-matched controls, although this short-term stimulatory effect is not evident if the test meal is delayed beyond 1 h. This time-course suggests that short-term stimulation of appetite may be mediated by the pharmacological action of alcohol on the appetite control system, either through enhanced orosensory reward or impaired satiety. In the long term, energy ingested as alcohol is additive to energy from other sources, suggesting that moderate alcohol consumption results in long-term passive over-consumption alongside short-term active over-consumption of energy through appetite stimulation. Despite the consistency of enhanced energy intake after moderate alcohol, evidence of an association between alcohol in the diet and obesity remains contentious, although the most recent results suggest that alcohol intake correlates with BMI. Future research needs to address this issue and clarify the mechanisms underlying appetite stimulation by alcohol.

Laboratory opossums (Monodelphis domestica) show extreme genetic variability in their responsiveness to dietary lipids; a great proportion of the genetic variability in responsiveness is due to a single major gene. To determine whether the major gene for dietary response detected by genetic analysis in opossums is responsive to dietary cholesterol or dietary saturated fat, or a combination of both, we used males and females of susceptible and resistant lines of laboratory opossums that were 5 to 7 months old. The animals were challenged with three different experimental diets (high-cholesterol diets with or without high saturated fat from lard or coconut oil) and plasma lipoproteins were measured. Plasma and VLDL+LDL-cholesterol concentrations increased several-fold when the animals were fed the diet containing elevated cholesterol (P>0·001) or elevated cholesterol and fat (P>0·001) and differed between the two lines when they were fed high-cholesterol diets with or without fat (P>0·001). Plasma HDL-cholesterol concentrations were higher (P>0·05) in animals of the resistant line than in the susceptible line when they were fed the basal diet (550 (sem 30) v. 440 (sem 20) mg/l) and when they were fed the low-cholesterol and high-fat diet (600 (sem 30) v. 490 (sem 30) mg/l). Dietary coconut oil and lard had similar effects on plasma lipoprotein cholesterol concentrations in the susceptible line of opossums. A reduction in dietary cholesterol by 50% with either the lard or coconut oil blunted the plasma cholesterol response. The results from the present studies suggest that the major gene for dietary response previously detected by genetic analysis in laboratory opossums affects the response to dietary cholesterol but not to saturated fat.

Probiotics (PRO) are known to modulate immunity in animals and human subjects and to inhibit colon carcinogenesis in experimental models, but the effects of synbiotics (SYN) are not well understood. Therefore, the effects of PRO (Lactobacillus rhamnosus GG and Bifidobacterium lactis Bb12), PRE (inulin-based enriched with oligofructose, 100g/kg) and SYN (combination of PRO and PRE) on the immune system of rats were investigated in the azoxymethane (AOM)-induced colon cancer model. After 33 weeks, rats with and without AOM treatment were killed and immune cells were isolated from spleen, mesenterial lymph nodes (MLN) and Peyer's patches (PP). AOM treatment significantly reduced natural killer (NK) cell-like cytotoxicity in control rats and in PRO- and PRE-supplemented rats. SYN supplementation prevented the AOM-induced suppression of NK cell-like cytotoxicity in PP compared with control rats (P<0·01). SYN and PRE supplementation stimulated IL-10 production in PP in these rats (P<0·01) and in MLN of rats not treated with AOM (P<0·05). Interferon-γ production in PP was decreased by PRO supplementation (PRO and SYN groups combined; P<0·05). Proliferative responsiveness of lymphocytes (PP) from AOM-treated rats was suppressed in SYN-supplemented rats (P<0·01). Overall, SYN supplementation in carcinogen-treated rats primarily modulated immune functions in the PP, coinciding with a reduced number of colon tumours. PRE and PRO provided in combination as SYN may contribute to the suppression of colon carcinogenesis by modulating the gut-associated lymphoid tissue.

Hordeum vulgare var. Himalaya 292 is a new barley cultivar with altered starch synthesis and less total starch but more amylose, resistant starch (RS) and total and soluble NSP including β-glucan. To determine its nutritional potential, young pigs were fed diets containing stabilised wholegrain flours from either Himalaya 292, Namoi (a commercial barley), wheat bran or oat bran at equivalent dietary NSP concentrations for 21 d. Serum total cholesterol was significantly lowered by the Himalaya 292 diet relative to wheat bran, indicating that Himalaya 292 retained its hypocholesterolaemic potential. In all groups SCFA concentrations were highest in the proximal colon and decreased towards the rectum. Digesta pH was lowest in the proximal colon and highest in the distal colon. Large-bowel and faecal pH were significantly lower in the pigs fed the barley and oat diets, indicating greater bacterial fermentation. Caecal and proximal colonic pH was lowest and SCFA pools highest in the pigs fed Himalaya 292. Total and individual SCFA were lowest in the mid- and distal colon of the pigs fed Himalaya 292 or oat bran. These data suggest the presence of more RS in Himalaya 292 and suggest that its fermentation was rapid relative to transit. Differences in faecal and large-bowel anaerobic, aerobic, coliform and lactic acid bacteria were relatively small, indicating a lack of a specific prebiotic action. These data support the potential of this novel barley cultivar to improve health through plasma cholesterol reduction and increased large-bowel SCFA production.

Diet can affect cognitive ability and behaviour in children and adolescents. Nutrient composition and meal pattern can exert immediate or long-term, beneficial or adverse effects. Beneficial effects mainly result from the correction of poor nutritional status. For example, thiamin treatment reverses aggressiveness in thiamin-deficient adolescents. Deleterious behavioural effects have been suggested; for example, sucrose and additives were once suspected to induce hyperactivity, but these effects have not been confirmed by rigorous investigations. In spite of potent biological mechanisms that protect brain activity from disruption, some cognitive functions appear sensitive to short-term variations of fuel (glucose) availability in certain brain areas. A glucose load, for example, acutely facilitates mental performance, particularly on demanding, long-duration tasks. The mechanism of this often described effect is not entirely clear. One aspect of diet that has elicited much research in young people is the intake/omission of breakfast. This has obvious relevance to school performance. While effects are inconsistent in well-nourished children, breakfast omission deteriorates mental performance in malnourished children. Even intelligence scores can be improved by micronutrient supplementation in children and adolescents with very poor dietary status. Overall, the literature suggests that good regular dietary habits are the best way to ensure optimal mental and behavioural performance at all times. Then, it remains controversial whether additional benefit can be gained from acute dietary manipulations. In contrast, children and adolescents with poor nutritional status are exposed to alterations of mental and/or behavioural functions that can be corrected, to a certain extent, by dietary measures.

Five experiments were carried out to extend knowledge of purine metabolism in the camel (Camelus dromedarius) and to establish a model to enable microbial protein outflow from the forestomachs to be estimated from the urinary excretion of purine derivatives (PD; i.e. xanthine, hypoxanthine, uric acid, allantoin). In experiment 1, four camels were fasted for five consecutive days to enable endogenous PD excretion in urine to be determined. Total PD excretion decreased during the fasting period to 267 (se 41·5)?μmol/kg body weight (W)0·75 per d. Allantoin and xanthine+hypoxanthine were consistently 86 and 6·1?% of total urinary PD during this period but uric acid increased from 3·6?% to 7·4?%. Xanthine oxidase activity in tissues (experiment 2) was (μmol/min per g fresh tissue) 0·038 in liver and 0·005 in gut mucosa but was not detected in plasma. In experiment 3, the duodenal supply of yeast containing exogenous purines produced a linear increase in urinary PD excretion rate with the slope indicating that 0·63 was excreted in urine. After taking account of endogenous PD excretion, the relationship can be used to predict purine outflow from the rumen. From the latter prediction, and also the purine:protein ratio in bacteria determined in experiment 5, we predicted the net microbial outflow from the rumen. In experiment 4, with increasing food intake, the rate of PD excretion in the urine increased linearly by about 11·1?mmol PD/kg digestible organic matter intake (DOMI), equivalent to 95?g microbial protein/kg DOMI.

The increase in fractional rate of protein synthesis (Ks) in the skeletal muscle of growing rats during the transition from fasted to fed state has been explained by the synergistic action of a rise in plasma insulin and branched-chain amino acids (BCAA). Since growing lambs also exhibit an increase in Ks with level of feed intake, the objective of the present study was to determine if this synergistic relationship between insulin and BCAA also occurs in ruminant animals. Six 30 kg fasted (72 h) lambs (8 months of age) received each of four treatments, which were based on continuous infusion into the jugular vein for 6 h of: (1) saline (155 mmol NaCl/l); (2) a mixture of BCAA (0·778 μmol leucine, 0·640 μmol isoleucine and 0·693 μmol valine/min·kg); (3) 18·7 μmol glucose/min·kg (to induce endogenous insulin secretion); (4) co-infusion of BCAA and glucose. Within each period all animals received the same isotope of phenylalanine (Phe) as follows: (1) l-[1-13C]Phe; (2) l-phenyl-[ring 2H5]-alanine; (3) l-[15N]Phe; (4) l-[ring 2,6-3H]Phe. Blood was sampled serially during infusions to measure plasma concentrations of insulin, glucose and amino acids, and plasma free Phe isotopic activity; biopsies were taken 6 h after the beginning of infusions to determine Ks in m. longissimus dorsi and vastus muscle. Compared with control (saline-infused) lambs, Ks was increased by an average of 40 % at the end of glucose infusion, but this effect was not statistically significant in either of the muscles sampled. BCAA infusion, alone or in combination with glucose, also had no significant effect on Ks compared with control sheep. Ks was approximately 60 % greater for vastus muscle than for m. longissimus dorsi (P>0·01), regardless of treatment. It is concluded that there are signals other than insulin and BCAA that are responsible for the feed-induced increase in Ks in muscle of growing ruminant animals.

Milk fat contains considerable amounts of saturated fatty acids, known to increase serum cholesterol. Little is known, however, about the relative effect of different milk products on risk factors for CHD. The aim of the present study was to compare the effects of Jarlsberg cheese (a Norwegian variety of Swiss cheese) with butter on serum lipoproteins, haemostatic variables and homocysteine. A controlled dietary study was performed with twenty-two test individuals (nine men and thirteen women) aged 23–54 years. The subjects consumed three isoenergetic test diets, with equal amounts of fat and protein, and containing either cheese (CH diet), butter+calcium caseinate (BC diet) or butter+egg-white protein (BE diet). The study was a randomised cross-over study and the subjects consumed each diet for 3 weeks, with 1 week when they consumed their habitual diet in between. Fasting blood samples were drawn at baseline and at the end of each period. Serum was analysed for lipids and plasma for haemostatic variables and homocysteine. Total cholesterol was significantly lower after the CH diet than after the BC diet (−0.27 mmol/l; P=0.03), while the difference in LDL-cholesterol was found to be below significance level (−0.22 mmol/l; P=0.06). There were no significant differences in HDL-cholesterol, triacylglycerols, apo A-I, apo B or lipoprotein (a), haemostatic variables and homocysteine between the diets. The results indicate that, at equal fat content, cheese may be less cholesterol increasing than butter.

Metabolic adaptations to variations in food supply are incompletely understood in ruminant animal adipose tissue (AT) and muscle. To explore this, we studied lipid metabolism and glucose transport potential in one internal and one external AT, as well as in one oxidative and one glycolytic muscle from control, 7 d underfed and 21 d refed adult cows. Refeeding increased (+79 to +307 %) the activities of enzymes involved in de novo lipogenesis (fatty acid synthase, malic enzyme, glucose-6-phosphate dehydrogenase) in perirenal and subcutaneous AT; underfeeding did not modify these variables. Underfeeding decreased the activities of lipoprotein lipase (LPL) in perirenal AT (−70 %) and cardiac muscle (−67 %), but did not modify the activities in subcutaneous AT and longissimus thoracis. Refeeding increased LPL activities in all tissues (+40 to +553 %) to levels comparable with (cardiac muscle) or greater than (AT, longissimus thoracis) those observed in control cows. Such variations in perirenal and cardiac muscle LPL activities did not result from variations in LPL mRNA levels, but suggest a post-transcriptional regulation of LPL in these nutritional conditions. Underfeeding did not modify GLUT4 contents in perirenal AT and muscles, while refeeding increased it only in perirenal AT (+250 %). Our present results contrast with previous results in rats, where LPL is regulated in opposite directions in AT and muscles, and GLUT4 is generally increased by fasting and decreased by refeeding in skeletal muscles. The present results highlight the bovine specificity of the response, which probably arises in part from peculiarities of ruminant animals for nutrient digestion and absorption.

The high dietary protein requirements of salmonid fish are met with fishmeal-based feed in commercial aquaculture. The sustainability of this practice is questionable and, therefore, the feasibility of substituting fishmeal with plant-based products needs to be investigated. We investigated growth and metabolism in rainbow trout (Oncorhynchus mykiss) fed a diet composed of a mixture of plant proteins compared with those fed a fishmeal-based diet. Using two-dimensional gel electrophoresis of liver protein extracts, we showed that the liver protein profile changed in response to the alteration in the diet. A number of metabolic pathways were identified as sensitive to the protein source substitution. These included pathways involved in primary energy generation, maintenance of reducing potential, bile acid synthesis, and transport and cellular protein degradation. Interestingly, the pathways shown to be affected in the present study were somewhat different from those identified in our previous work with soyabean-based-protein replacement of fishmeal, with the effects on the abundance of several stress response proteins notably absent. We conclude, therefore, that the metabolic effects of plant protein replacement in aquaculture feed varies with plant-protein source.

The ‘malnutrition universal screening tool’ (‘MUST’) for adults has been developed for all health care settings and patient groups, but ease of use and agreement with other published tools when screening to identify malnutrition requires investigation. The present study assessed the agreement and the prevalence of malnutrition risk between ‘MUST’ and a variety of other tools in the same patients and compared the ease of using these tools. Groups of patients were consecutively screened using ‘MUST’ and: (1) MEREC Bulletin (MEREC) and Hickson and Hill (HH) tools (fifty gastroenterology outpatients); (2) nutrition risk score (NRS) and malnutrition screening tool (MST; seventy-five medical inpatients); (3) short-form mini nutritional assessment (MNA-tool; eighty-six elderly and eighty-five surgical inpatients); (4) subjective global assessment (SGA; fifty medical inpatients); (5) Doyle undernutrition risk score (URS; fifty-two surgical inpatients). Using ‘MUST’, the prevalence of malnutrition risk ranged from 19–60% in inpatients and 30% in outpatients. ‘MUST’ had ‘excellent’ agreement (κ 0.775–0.893) with MEREC, NRS and SGA tools, ‘fair–good’ agreement (κ 0.551–0.711) with HH, MST and MNA-tool tools and ‘poor’ agreement with the URS tool (κ 0.255). When categorisation of malnutrition risk differed between tools, it did not do so systematically, except between ‘MUST’ and MNA-tool (P=0.0005) and URS (P=0.039). ‘MUST’ and MST were the easiest, quickest tools to complete (3–5 min). The present investigation suggested a high prevalence of malnutrition in hospital inpatients and outpatients (19–60% with ‘MUST’) and ‘fair–good’ to ‘excellent’ agreement beyond chance between ‘MUST’ and most other tools studied. ‘MUST’ was quick and easy to use in these patient groups.

The effect of energy density (ED) on energy intake (EI) has been assessed in short-term and long-term experiments. In the short term, it was found that ED affects EI directly in situations when the subjects cannot estimate the ED of the food; then subjects mainly monitor the weight of the food ingested. In the long term, the effects of ED on EI are modulated. Average daily EI appears to be related to ED of the food and drinks when ED is determined by specific macronutrients, but not when ED is only determined by the weight of water. Thus, the short-term effect ED has on EI cannot be extrapolated to the long term, because a possible dominating effect of the weight of water determining ED undoes the relationship of ED with EI. Moreover, in the long-term portion sizes are used to compensate for correctly estimated ED, resulting in less variation in EI than ED alone would imply. Finally, dietary restraint compensates for the effect of a relatively high ED on daily EI, whereas dietary unrestraint compensates for the effect of relatively low ED on daily EI. We conclude that the short-term effect of ED on EI is modulated by the effect of water on ED, and compensated for by the effect of dietary restraint and adapted portion sizes.