To test the proposition that sheep are able to select a diet that meets their crude protein (N × 6.25; CP) requirements, feeds L, A, B, C and H with the same energy content (11 MJ metabolizable energy/kg feed) but different CP contents (78, 109, 141, 172 and 235 g CP/kg fresh feed respectively) were formulated. In addition, feed U, which was feed L plus 21.4 g urea/kg (CP content 132 g/kg), was also made. The feeds were offered ad lib. either singly (n 4 per treatment) or as a choice between feed H and another feed (pairs LH, AH, BH, CH and UH; n 9 per feed pair) to individually penned Suffolk × Scottish mule wether lambs, over the live-weight range 25–45 kg. On the single feeds the rates of live-weight gain were 273, 326, 412, 418, 396 and 407 g/day (SE of difference (SED) 34; P < 0.01) and protein (excluding wool) gain were 27, 32, 44, 45, 41 and 39 g/d (SED 4; P < 0.001) for feeds L, A, B, C, H and U respectively. When sheep were given a choice between a feed below (L or A) and a feed above their CP requirements (H; as judged by the single-feeding treatments) the CP concentration selected was not different between the two pairs: 131 (SE 4) v. 133 (SE 4) g CP/kg feed for pairs LH and AH respectively. On the choices BH and CH (a choice between two feeds above requirements) the feed lower in CP was constantly preferred (874 (SE 33) and 910 (SE 33) g feed B and C respectively per kg total feed intake; CP selected was 157 and 178 g CP/kg respectively). However, this was not the case with the UH choice on which sheep consumed only 599 (SE 61) g feed U/kg total feed intake, resulting in a selection of a higher CP in their diet (173 g CP/kg). The live-weight gains of the animals given a choice between two feeds were 416, 387, 415, 410 and 383 g/d (SED 37) and protein gains were 45, 40, 46, 50 and 43 (SE 7) for pairs LH, AH, BH, CH and UH respectively, which were comparable with the best performance achieved on a single feed. The results suggest that sheep were able to select a diet that meets their CP requirements and avoid, at least to a certain extent, excess of protein intake. It is also possible that sheep discriminate against a property of feed U, such as an excess of urea, when this feed is paired with a feed high in CP.

Two formulas were derived to estimate the energy content of the human body which use only body mass, total body water by 3H2O dilution space and body minerals assessed by anthropometry. The formulas were tested in a body composition database of 561 patients and 151 normal volunteers using established metabolizable energy values for protein, fat and glycogen. Total body protein was determined by in vivo neutron activation analysis (IVNAA), body water by dilution of tritium and body minerals from skeletal frame size. Body glycogen was assumed to be 14.6 % of the mineral component. Body fat was obtained by difference, body mass less the sum of water, protein, minerals and glycogen. The standard deviation in the estimate of body energy content was 30 MJ or 4.1 % of the energy content of reference man. Two formulas for body energy content were derived by regression with body mass, total body water and body minerals or height. Two formulas for energy density and formulas for percentage body fat were similarly derived.

In twenty-eight healthy subjects, ten men and eighteen women, with a range in body mass index (BMI) of 17.9–31.6 kg/m2 and an age range 20–60 years, body composition was estimated by dual-energy X-ray absorptiometry (DEXA), skinfold anthropometry (SFA) and bioelectrical impedance analysis (BIA) of the ‘whole body’and body segments. In thirteen subjects muscle mass was also estimated by 24 h urinary creatinine excretion. The relationship between fat-free mass (FFM) determined by DEXA and the impedance index of each body segment (calculated as Iength2/impedance (Z)) was analysed. The strongest correlation was between FFM (DEXA) and height2/‘whole-body’Z (Zw) (r 0.97 for the combined sexes, standard error of estimate (SEE) 2.72 kg). Separate prediction equations were found to be necessary for males and females when estimating FFM from BIA measurement of the arm (for men, r 0.93, SEE 1.98 kg; for women, r 0.75, SEE 2.87 kg). Muscle mass derived from 24 h creatinine excretion showed weak correlation with FFM (DEXA) (r 0.57, P = 0.03) and no correlation with FFM (SFA). FFM (SFA) correlated well with both FFM (DEXA) (r 0.96, SEE = 3.12 kg) and with height2/Zw (r 0.92, SEE 4.52 kg). Measurement of the impedance of the arm offers a simple method of assessing the composition of the whole body in normal individuals, and it appears comparable with other methods of assessment.

Fat-free mass (FFM) was estimated in forty-seven premenopausal Chinese women, aged 18–43 years, from anthropometric data (skinfolds, body mass index (weight/height2; BMI)) or bioelectrical impedance, using several prediction formulas for body composition from the literature, and values compared with the mean of these three individual methods used as a frame of reference. In thirty-six women these values could be compared with FFM calculated from total body water (TBW) determined by D2O dilution. The prediction formulas used were developed from studies on Caucasian adults and their validity will have to be shown in populations with different ethnic backgrounds. The mean difference between FFM predicted from BMI and the frame of reference was 0.1 kg (95 % confidence interval (CI) -0.1, 0.4), from bioelectrical impedance it was 0.5 kg (95% CI 0.3, 0.7), and from skinfolds it was -0.6 kg (95% CI -0.9, -0.4). The mean difference between FFM calculated from TBW and the frame of reference was higher (2.2 kg, 95 % CI 1.2,3.3). The results of the present study indicate that the three methods may be valid for predicting body composition in adult Chinese females, but further research is needed on development and cross-validation of prediction equations for body composition for Chinese.

Nutritional assessment and adequacy of spontaneous dietary intake was evaluated in thirty-seven clinically stable hospitalized patients with alcoholic liver cirrhosis. About two-thirds of the patients had ascites or oedema, or both, and, therefore, body weight could not be used for assessment of nutritional status. Lean body mass (LBM; measured by three consecutive 24 h creatinine excretions) was 62 (range 40–95)% of reference values, mid-arm-muscle area (MAMA) was 70 (range 43–115)% and triceps skinfold (TSF) was 45 (range 20–113)% of reference values (all median values). In patients without ascites or oedema, or both, there was a rectilinear correlation between body weight and LBM and between body weight and MAMA (r 0.93 and 0.85 respectively). In patients with ascites or oedema, or both, the correlation between body weight and LBM was poor as could be expected. We suggest that LBM is a useful measure of nutritional status when body weight is unreliable because of ascites or oedema, or both. Energy balance for the group was calculated from energy intake recorded by a 24 h dietary recall and energy expenditure calculated by the factorial method. Median intake was 102 (range 34–176)% of expenditure. N loss was calculated from the average of three 24 h urea excretions. Protein intake was calculated from the 24 h dietary recall. The N balance was positive in the patients as a group (median intake was 120 (range 26–183)% of output). The most malnourished patients tended to have the most positive N balance which was due to a significantly lower N excretion. The protein requirement for N balance was 0.83 (SE 0.05) g/kg per d and only at an intake above 1.20 g/kg per d were all patients in positive N balance. The median intakes of thiamin, folacin, vitamin D, vitamin E, Mg, and Zn were judged to be insufficient. It is concluded that impaired nutritional status is common among patients with liver cirrhosis, even in a stable clinical condition. It is suggested that nutritional status in these patients is evaluated by dietary recalls, in combination with measurement of body weight in patients without ascites or oedema, or both, or in combination with determination of LBM by three 24 h creatinine excretions in patients with ascites or oedema, or both. Criteria for selection of patients that might benefit from nutritional therapy are discussed.

A factorial 3 × 3 experiment was conducted with chicks to investigate the effect of manipulating crude protein (N × 6.25) intake (CPI) and metabolizable energyintake (MEI) simultaneously, in the range low to high (including adequate) levels with regard to the respective requirements, on whole-body protein turnover and its contribution to total heat production. The fractional rate of whole-body protein synthesis was increased curvilinearly by increasing MEI or CPI from low to high levels. In terms of absolute rates whole-body protein synthesis was enhanced by increasing MEI from low to adequate levels, the effect being greater at adequate and high CPI than at low CPI. The effect of varying CPI and MEI on whole-body protein degradation was similar, but less sensitive, to that on whole-body protein synthesis. Increasing MEI from low to high levels elevated totalheat production at all CPI levels. There were no interactive effects of varying CPI andMEI on the contribution of whole-body protein synthesis to total heat production, and in general the contribution increased with increasing CPI and decreased with increasing MEI.The contribution of whole-body protein synthesis to total heat production fell within a small range from 11.2 to 16.5%.

The aim of the present study was to investigate the effect of soya-bean protein on growth and muscle metabolism in fish. Cod, Gadus morhua, were fed on a fish-feed formula with the high-quality fish-meal protein being replaced by 100, 200 or 300 g soya-bean protein/kg fish-meal protein. The feeding experiment lasted for 43 d at a water temperature of 7–8º and a sea water salinity of 3.5%. At the 200 g/kg level of soya-bean protein, food intake and growth rate were similar to those of the controls. At the 300 g/kg level of soya-bean protein, food intake was diminished by 6 % and growth by 67 % relative to control levels. In muscle, sarcoplasmic protein (/g wet weight) was significantly decreased by 14%. Myofibrillar protein (/g wet weight) was unchanged. Levels of RNA in the myofibrillar fraction decreased at all three levels of soya-bean protein, and that of the sarcoplasmic fraction decreased at the highest level of legume-protein. With increased levels of soya-bean protein, RNA: DNA declined by 18% from 1.88 to 1.54. The contractile protein myosin heavy chain (/mg protein and /g wet weight) and myosin heavy chain-specific mRNA (/mg RNA) were not significantly affected by dietary conditions. Expressed per g wet weight, the decline by 21 % of the specific mRNA depended on the total RNA content which decreased with the increase in soya-bean protein. Acid proteinase activity was lowest at the 200 g/kg level, showing a decrease of 23%. Glycogen content fell by 46% at both the 200 and 300 g/kg level of dietary soya-bean protein. The results show that muscle metabolic functions responded to the dietary plant protein before there were any measurable changes in growth rate. From the results it is concluded that 200 g/kg or less of the high-quality fish-meal protein may be replaced by soya-bean protein in a fish-feed formula.

Rumen-fistulated lactating cows were individually fed on hay or silage and intakes were monitored during 3 h treatment periods and for 2 h after. Each experiment used five, six or seven animals and the treatments were applied in a Latin Square design. Sodium acetate infusions of 1·8–11·0 mol in 4.5 litres water caused a dose-related depression in hay intake, the extent being 82 g dry matter (DM)/mol infused (P < 0·01). Sodium acetate infusions of 6·0–15·0 mol in 4·5 litres water caused a dose-related depression in silage intake of 118 g DM/mol infused. Rumen fluid pH for both diets was unaffected by treatment. Acetate and Na concentrations were increased and significantly negatively correlated with intake of both diets. Infusions of 2–8 mol sodium propionate caused a dose-related depression of hay intake which was significant when cow and day effects were accounted for. Sodium propionate infusions of 4–8 mol significantly depressed silage intake by 140 g DM/mol infused (P < 0·001). Rumen fluid pH was unaffected by treatment while propionate and Na concentrations were elevated and significantly negatively correlated with intake for both diets. Inflation of a rubber balloon in the rumen with 12.5–20 litres warm water resulted in a dose-dependent depression in hay intake of 66 g DM/1 distension (P < 0·05). There was significant overeating during the 2 h following the 20 litre treatment. With silage, 15–25 litres of balloon distension for 3 h resulted in a dose-dependent depression in intake of 28 g DM/l distension (P < 0·001). There was no significant overeating during the 2 h following distension. When given in physiological amounts, at the lower end of the range used in these experiments, acetate, propionate and distension of the rumen did not significantly affect hay intakes. However, in each case the linear relationship between intake depression and level of treatment suggested that these factors could contribute to the control of feed intake.

In order to test the hypothesis that negative leedback signals from abdominal receptors are integrated in an additive manner in the control of voluntary food intake, cows with rumen fistulas were given intraruminal infusions of sodium acetate or sodium propionate, cr both, with or without distension of the rumen by balloon. Intakes were monitored during the 3 h experimental period and for 2 h after and samples of rumen fluid were taken for estimation of short-chain fatty acid concentrations and osmolality. Six cows in mid-lactation were fed on hay and concentrates and given, into the rumen. 5.5 mol sodium acetate, 5.2 mol sodium propionate and 7.51 of distension. Compared with the control (water infusion), neither acetate, propionate nor distension significantly depressed hay intake when given separately. When given in combination, however, the following significantly depressed intake during the 3 h treatment period: propionate + distension, acetate + distension, acetate + propionate + distension. Seven cows in early lactation were fed on silage and concentrates and given, into the rumen, 9.0 mol sodium acetate, 4.0 mol sodium propionate and 10.0 litres of distension. Again, none of the three given alone depressed silage intake to a significant extent during the 3 h treatment period, whereas the following combinations had a significant effect: propionate + distension, acetate + distension, acetate + propionate + distension. Basal rumen osmolalities were similar for the two types of feed but infusion of the sodium salts caused a very much greater increase with silage than with hay. The results are discussed with regard to the implications for our understanding of the control of voluntary intake and the likely role of chemo-, osmo- and mechano-receptors.

The present study examined the effect of urea-N supplementation of a N-deficient diet on digestion and metabolism in the rumen. Five Rasa Aragonesa ewes, each fitted with a rumen cannula, were offered alkali-treated barley straw ad lib. alone or supplemented continuously via the cannula with four levels of urea-N (3, 6, 9 and 12 g/d). Rumen NH3 concentrations increased in response to urea infusion (6–128 mg/l; P < 0.001). At the highest level of rumen NH3 concentration there was a significant increase, compared with the unsupplemented treatment, in dry matter (DM) intake (846–1206 g/d; P < 0.001) and apparent digestibility of DM (0.38–0.43), organic matter (0.38–0.45) and neutral-detergent fibre (0.41–0.49; P < 0.01). Rumen outflow rates of particulate matter and potential DM disappearances, assessed using nylon bags, were not affected by the experimental treatments, although fractional rate of DM disappearance increased significantly with increasing levels of urea infusion (2.4–4.6 per h). Urinary excretion of total purine derivatives increased with N supplementation, although the response was exclusively due to an increase in allantoin excretion (26.9–66.4 mg/kg live weight (W)0.75 per d; P < 0.001). Xanthine, hypoxanthine and uric acid excretion rates were constant, averaging 1.8 (SE 0.17); 5.4 (SE 0.21) and 7.2 (SE 0.36) mg/kg W0.75 per d respectively. The maintenance of a minimum rumen NH3 concentration (approximately 50 mg/l) was necessary to avoid significant reductions in DM intake and fermentation rate. Higher levels, however, may further increase microbial N flow at the duodenum, as suggested by the response in urinary allantoin excretion over the range of rumen NH3 concentrations.

The fate of a small oral dose of protein given to overnight-starved rats was studied. After 3 h, 62 % of the protein amino acids had been absorbed. Most of the absorbed N went into the bloodstream through the portal in the form of amino acids, but urea and ammonia were also present. About one-quarter of all absorbed N was carried as lymph amino acids. The liver was able to take all portal free ammonia and a large proportion of portal amino acids, releasing urea. The hepatic N balance was negative, indicating active proteolysis and net loss of liver protein.

The kinetics of 3-methylhistidine (3MH) metabolism in four crossbred lambs were studied. Each lamb was injected with an intravenous dose of 3-[2H3]methylhistidine (d3-3MH) and the stable isotope disappearance in plasma and appearance in both urine and muscle were measured. Immediately after the administration of tracer there was a phase of rapid disappearance of tracer from the plasma, which was followed by a more gradual decrease in d3-3MH from the plasma during the last 4 d of the experiment. A minimum of three exponentials was required to describe the plasma decay curve adequately. The kinetic model of 3MH in the whole animal was constructed by using the SAAM/CONSAM computer modelling program. Two different configurations of a three-compartment model are described: (1) a simple three-pool model, in which plasma kinetics were entered into pool 1 out of which they had one undefinable exit; (2) a plasma-urinary three-pool model with two exits, in which the urinary kinetics were entered as an exit out of pool 1 and required a second exit out of pool 3 to produce an adequate fit. In addition, muscle kinetics from biopsies of the longissirnus dorsi were entered into either pool 2 or 3 using the plasma-urinary model. Steady-state mass and transport rate values were obtained for each model construct described, and a de novo production rate corresponding to a fractional breakdown rate of myofibrillar protein of approximately 5%/d was also calculated. The model predicted that only 15% of 3MH was excreted in urine as free 3MH, which is consistent with current knowledge of 3MH excretion in sheep. The simple three-pool plasma kinetic model, therefore, could be used to estimate, by a relatively simple injection-sampling technique, the extent of muscle protein turnover in lambs.

The effects of amount and type of dietary fish proteins on plasma and liver cholesterol concentrations were evaluated in female rats. The isonitrogenous diets used contained 10 g cholesterol/kg and were carefully balanced for residual fat, cholesterol, Ca, Mg and P in the protein preparations. Cod meal, soya-bean protein or casein was incorporated into the diets as the only source of dietary protein a t three levels: either 24,48 or 72 g N/kg diet. Extra protein was added to the diet at the expense of the glucose component. In a second experiment soya-bean protein, casein, cod meal, whiting meal or plaice meal was added to the diet at a level of 24 g N/kg. When compared with casein, cod meal and soya-bean protein decreased plasma and liver cholesterol concentrations. A further cholesterol-lowering effect was achieved by increasing the proportion of either soya-bean protein or cod meal in the diet. Substitution of casein for glucose did not influence plasma and liver cholesterol concentrations. Plaice meal in the diet produced lower group mean plasma cholesterol concentrations than did whiting meal. In rats fed on the diet containing plaice meal, liver cholesterol concentrations were significantly lower than those in their counterparts fed on either cod meal or whiting meal. The present study demonstrates that different fish proteins in the diet have different effects on cholesterol metabolism and that the cholesterol-influencing properties of cod meal can be enhanced by the incorporation of higher proportions of this protein in the diet.

To study the effects of medium-chain triacylglycerols (MCT) on maternal lipid metabolism and pup growth, MCT (200 g/kg) were incorporated into a commercial chow diet and fed to lactating rats for 8–10 d. The results were compared with similar diets containing sunflower oil (polyunsaturated fatty acids; PUFA), tristearin (saturated fatty acid) or triolein (monounsaturated fatty acid). There was decreased food and energy intake with the MCT diet and this was accompanied by decreased (35%) pup growth. All the high-fat diets inhibited lipogenesis in vivo in the lactating mammary gland, the order of effectiveness being PUFA > triolein > tristearin > MCT. Only the MCT diet increased the rate of hepatic lipogenesis (180%). Experiments feeding an MCT meal containing [l-14C]octanoate indicated that very little (3–4%) of the C was present in mammary gland lipid, unlike the findings with [l-14C]triolein meal (40%). The major portion (65%) of the absorbed [l-I4C]octanoate was oxidized to 14CO2. There was no evidence for adaptation of the mammary gland to increased dietary lipid uptake on the triolein or MCT diets. It is concluded that the decreased pup growth on the MCT diet is due in part to the decreased energy intake and to the inability of dietary medium-chain fatty acids to provide substrates for milk lipid synthesis.

The role of the soluble non-starch polysaccharide pectin in the prevention of oxidative damage induced by peroxy, superoxide and hydroxyl radicals to the rat jejunal mucosa was studied. The oxidative stress was introduced to the rat jejunal mucosa by means of a closed-loop perfusion system and was characterized biochemically by monitoring the enterocyte activity of the enzyme lactate dehydrogenase (EC 1·1·1·27) and the K+ level. Aqueous solutions of pectin were perfused into the rat jejunum before the oxidative stress inducers. The possible protection effect was evaluated by comparing the mucosal integrity (as measured by biochemical variables) to the values obtained after perfusion with the oxidative stress inducers only. We found that: (a) mucosal damage was detected following the perfusion of peroxy and hydroxyl radicals in the rat jejunum, but not following perfusion of the superoxide radical; (b) a significant reduction in the mucosal damage was noted when pectin was perfused before the perfusion with the peroxy radical induction; (c) full protection against the mucosal damage induced by hydroxyl radicals was achieved when pectin was perfused before the damage induction.

The effects of folate sufficiency and deficiency in three pathways of folate metabolism were studied in 2- and 3-week-old broiler chicks. Erythrocyte phosphoribosylpyrophosphate concentrations and dihydro- folate reductase (EC 1.5.1.3) activity were significantly elevated in folate deficiency. Percentage incorporation of deoxyuridine into bone marrow DNA was reduced in folate deficiency. There was a trend towards reduced liver dihydrofolate reductase activity in deficient chicks. These studies identify further biochemical criteria that can be used to assess folate status of chicks.

Three experiments were carried out to investigate the effects of supplemental dietary 1·25-dihydroxycholecalciferol (1·25(OH)2cholecalciferol) and a low dietary Ca:P ratio on the occurrence of tibial dyschondroplasia (TD) in 3-week-old broilers. Histopathology was used to diagnose TD. In the first experiment, feeding a diet containing 7·5 g Ca and 7·6 g P/kg gave a higher incidence of TD than a control diet containing normal amounts of Ca and P (12 and 6 g/kg respectively). Increasing the dietary supplement of cholecalciferol in the imbalanced diet prevented rickets but did not decrease the incidence of TD. In the second experiment, supplementing the imbalanced diet with 10 μg 1·25(OH)2cholecalciferol/kg prevented TD completely but also gave a slight growth depression. In the third experiment the imbalanced diet was supplemented with 0, 2·5, 5 or 10 μg 1·25(OH)2 cholecalciferol/kg. The supplement of 2·5 μg/kg depressed and the higher supplements prevented the occurrence of TD, this time without a growth depression. Feeding the 10 μg/kg supplement for the first week only did not prevent TD. Plasma total Ca, inorganic P and alkaline phosphatase (EC 3·1·3·1) were unaffected by diet but 1·25(OH)2cholecalciferol was higher on the imbalanced than on the control diet. Supplementation of the imbalanced diet with 1·25(OH)2cholecalciferol did not increase plasma levels. It is concluded that 1·25(OH)2cholecalciferol is exerting a powerful biological effect in this model of TD, but the mechanism is unclear.

The effect of Ascaris lumbricoides infection on retinol absorption was investigated in young children from a slum area of Dhaka City, Bangladesh. Twenty-four children aged 4–10 years were screened and in every case eggs of either Ascaris, Trichuris or hookworm were isolated from the stool. The average serum retinol was 0.91 (sd 0.35) μmol/l and sixteen children had levels below 1.05 μmol/l. This compared with a serum retinol concentration of 1.70 (sd 0.52) μmol/l in five reference children from a more privileged social background. An oral dose of retinol (41.8 μmol) was given, to ten children in whom the concentration of Ascaris eggs in the stool varied. Less than 1% of the supplement could be recovered in the stools collected over the following 48 h. Ascaris worms were isolated from the stool and assayed for retinol content. In no case was retinol detected in the worms. These findings do not support the contention that infection with Ascaris predisposes to malabsorption of vitamin A.

The ability to hydrolyse and absorb pteroylpolyglutamates (PteGlun) included in a standard meal in mothers who had given birth to an infant with a neural tube defect was tested by comparing them with mothers who had not had any infants with this defect. When compared with control mothers working in the research unit in which the study was performed, case mothers had significantly lower baseline serum and erythrocyte folate levels, and smaller increases in serum folate following the meal containing PteGlun. However, all estimates of folate were similar when case mothers were compared with a group of mothers who were friends of the case mothers. The results show that the higher the baseline levels of serum and erythrocyte folate the greater the increase in serum folate after the test meal. Fitting a model for the serum folate response curve resulted in coefficients which differed significantly between case mothers and all control mothers. We conclude that intestinal hydrolysis of PteGlun taken orally is not impaired in mothers who have had infants with neural tube defects when compared with control mothers with similar baseline folate levels, although the curves describing the response to the meal for the two groups do differ significantly. Further investigation is required to determine the mechanism underlying this difference.