1. A high incidence of vitamin B12 or folate deficiency, or both, may be found in the elderly, particularly those in hospital. This report concerns fifty cases detected in an inner-city-area geriatric unit during the course of routine clinical investigation. The majority had none of the classical haematological signs of vitamin B12 or folate deficiency, and all the patients reported had a mean corpuscular volume (MCV) of less than 100 fl.

2. There was a significant negative correlation between the MCV and the erythrocyte folate (P< 0.01), supporting earlier published work using a low serum folate as an index of folate deficiency.

3. There was no correlation between the MCV and the serum vitamin B12. Published work differs on this point.

4. Serum iron, total Fe-binding capacity and percentage Fe saturation results were available in forty patients in this series. There was a significant positive correlation between the serum Fe and the MCV (P<0.01) and 34% of patients had haematological evidence of Fe deficiency. In the majority, however, there was no evidence that associated Fe deficiency had masked the haematological signs of vitamin B12 or folate deficiency.

5. More attention should be paid to the problem of ‘masked’ vitamin B12 and folate deficiency in the elderly. There is a case for routine screening of the elderly for vitamin B12 and folate deficiency irrespective of the MCV.

1. The excretion of aliphatic amines, methylamine, dimethylamine and trimethylamine in the urine and faeces of rats fed on a control diet and diets supplemented with creatinine, lecithin or choline were measured over a 14 d feeding period.

2. The rats were then killed and concentrations of amines in small and large intestinal contents measured.

3. Adding creatinine to the diet resulted in a significant increase of methylamine excretion in the faeces and urine. The amount of methylamine found in all parts of the intestine increased, especially in the caecum.

4. Adding lecithin to the diet resulted in an increase in the methylamine excretion only, and no change in the concentrations of amines found in the intestine, except for trimethylamine which was significantly increased in the caecum and colon.

5. Adding choline to the diet resulted in a significant increase in excretion of trimethylamine and, to a lesser extent, methylamine. The levels of amines found in the gut increased, dimethylamine being increased in the small bowel, and methylamine and trimethylamine in the caecum.

1. Metabolism, in broiler chicks, of DL-2-hydroxy 4-methylthiobutanoic acid (DL-HMB), DL-methionine and L-methionine was compared in vivo using 14C-labelled tracers.

2. The distribution of L-[1-14C]methionine and DL-[1-14C]HMB in the major body tissues was examined for a period of 120 min after administration.

3. The relative oxidation (14CO2, exhaled), excretion and incorporation into tissue protein of L-[l-14C]methionine, DL-[l-14C]methionine and DL-[1-14C]HMB were measured in fed birds.

4. Tissue distribution of L-[1-14C]methionine and DL-[1-14C]HMB differed during 60–90 min following administration.

5. The production of 14CO2, from each of the tracers was similar but excretion of 14C-labelled material was very different with the greatest excretion from DL-[1-14C]HMB and the least from L[1-14C]methionine.

6. The incorporation of 14C into tissue proteins varied with the tracer given and the tissue examined. Liver and kidney had equivalent incorporation from each of the tracers while other tissues examined showed lower incorporation from DL-[1-14C]methionine and DL-[1-14C]HMB.

7. The results show that DL-HMB, D-methionine and L-methionine are metabolized differently in vivo and that they are excreted in differing proportions. There is also a difference in the ability of each to act as a precursor for protein synthesis in tissues other than liver.

1. Breath hydrogen and methane were determined by gas chromatography in eleven normal individuals given a low-fibre, mixed diet (control) and after ingestion of 20–50 g Palatinit®/d, an equimolar mixture of D-glucosyl-α(1 → 1)-D-mannitol and D-glucosyl-α(1 → 6)-D-glucitol (Isomalt®).

2. A linear relation was found (r 0.85; P < 0.001) between the amount of Palatinit ingested and breath H2 per 10 h in subjects who did not exhale methane. If methane was formed in addition to H2, the sum of both gases followed a linear dose-effect relation.

3. The mouth-to-caecum time, indicated by the first increase in breath H2, after ingestion, was shortened by about half, yet no sign of diarrhoea was observed. Stool weight and stool frequency did not change significantly.

4. The linear relation between a dose of 20–50 g Palatinit and exhalation of H2 (eventually plus methane) indicated that a relatively constant fraction of the dose given underwent cleavage and absorption in the small intestine, the remainder being transported into the large bowel. Microbial gas formation in the colon as well as the fractional transfer of these gases into the expiratory air occurred at fixed proportions, thus allowing an insight into colonic microbial contributions to carbohydrate utilization in the human large bowel.

1. Intestinal absorption of sorbitol was studied in a duodeno-jejunal loop of anaesthetized rats. The acute effects of exogenous sorbitol on glucose homeostasis were also evaluated in male and female rats.

2. In the presence of lumen concentrations of sorbitol ranging from l μM to 200mM, a fairly constant low percentage (about 12%) of the loop's contents was absorbed after 30 min. This amount increased only slightly with time, but this was not due to sorbitol accumulation in the mucosal layer of the loop.

3. 3-O-methylglucose was absorbed much more quickly than sorbitol, but did not interfere with sorbitol absorption. The latter was not impaired by omission of lumen sodium ions nor by phloridzin, both of which inhibited 3-O-methylglucose absorption.

4. Gastric administration of sorbitol did not affect plasma glucose or insulin levels. Glucose or sucrose administration caused a similar rise in plasma glucose, but the increase in plasma insulin levels was larger after glucose than after sucrose administration.

5. Intravenous administration of sorbitol slightly increased plasma glucose and insulin levels. These changes were, however, considerably smaller than those occurring after glucose administration.

6. In the normal rat, intestinal absorption of sorbitol is passive and proceeds at a low rate. Acute oral administration of sorbitol does not affect glucose homeostasis, which is only slightly disturbed by a large intravenous load of sorbitol.

1. The metabolism of 65Zn administered intramuscularly (Expt 1) or enterally (Expt 2) at the beginning of pregnancy in rats given a control or marginal-Zn diet was measured. In Expt 2 a comparison was also made between pregnant and non-pregnant rats. The loss of 65Zn (assumed to represent labile body Zn) was markedly reduced in animals fed on a marginal-Zn diet compared with controls, and this effect occurred very rapidly, i.e. within 48 h of introducing the marginal-Zn diet. Pregnancy itself had a much less important effect on 65Zn turnover than diet. Transfer of 65Zn to the litter was significantly greater in the animals fed on a marginal-Zn diet compared with controls but total Zn transfer was reduced.

2. The effect of length of time on a marginal-Zn diet on fetal growth and composition was examined. Compared with controls, fetal weight was significantly greater in litters from mothers fed on a marginal-Zn diet during the last 4, 7 or 14 d of pregnancy, but no different in litters from mothers fed on a marginal-Zn diet throughout pregnancy. There were no differences in the proportions of protein or fat in the fetuses from mothers fed on the control or marginal-Zn diets but the Zn concentration was lower in litters from mothers fed on a marginal-Zn diet during part or ail of the pregnancy when compared with controls.

3. The transfer of 65Zn from mothers to litters during birth and the first 3 d of lactation was measured. There were no differences in maternal or litter 65Zn just before or just after birth, but within 72 h maternal 65Zn had significantly decreased and litter 65Zn increased. Increases in litter size were associated with greater total litter 65Zn but reduced individual fetal 65Zn.

4. These experiments demonstrate the importance of an adequate daily supply of Zn during pregnancy. Although there is room for adaptation to a marginal-Zn intake (by reducing Zn excretion) the maintenance of Zn homeostasis is only possible in the absence of other forms of stress, such as pregnancy, to the body. The consequence of insufficient Zn at times of rapid fetal growth on carbohydrate and lipid metabolism warrants further investigation.

1. The fermentative breakdown of one resistant type of dietary fibre (wheat bran) and one easily-fermented fibre (low-methoxyl pectin) was studied with respect to the length of the adaptation period and fibre level in the diet. The breakdown of the resistant fibre was also studied regarding the protein level in the diet and particle size of the fibre.

2. Prolongation of the adaptation period from 4 to 18 d decreased the faecal dry weight considerably. The excretion of dietary fibre however, was similar, whereas a decrease in faecal nitrogen excretion could be seen.

3. A level of dietary protein of less than 50 g/kg impaired the fermentation of wheat-bran fibre, whereas a level higher than 100 g protein/kg did not further increase the degree of fermentation of the fibre.

4. The particle size did not change the fermentability of the fibre, equal amounts of the main components of coarse and milled bran being excreted in faeces.

5. Two different levels of wheat-bran fibre (48 and 96 g/kg) in the diet did not influence the fibre breakdown. Similar results were obtained with two levels of fibre from low-methoxyl pectin (42 and 84 g/kg), but a tendency towards a decreased percentage of faecal excretion of uronic acids was seen at the lower level of low-methoxyl pectin.

1. Protein-deficient weanling rats fed on a 30 g casein/kg diet for 3 weeks lost albumin but maintained the level of serum α-1-antitrypsin, the most abundant protease inhibitor in blood.

2.α-1-Antitrypsins from malnourished rats and control rats (given 250 g casein/kg diet) differed; the protease inhibitor from protein-deficient animals: (1) was more acidic, (2) appeared slightly larger (57400 v. 56000 daltons) on sodium dodecyl sulphate (SDS)-polyacrylamide gels, (3) had a more acidic Pi type and increased anodal mobility at pH 8.9, (4) bound more concanavalin-A and contained more carbohydrate, specifically two to three extra sialic acid residues. The amino sugar and neutral sugar contents of both preparations of α-1-antitrypsin were the same.

3. Analysis of the products of cyanogen-bromide cleavage revealed that α-1-antitrypsin preparations from protein-deficient rats contain an extra glycopeptide that was not present in α-1-antitrypsin from control animals.

4. In vivo studies showed that the increased sialic acid content of α-1-antitrypsin of protein-deficient rats did not alter the half-life of the molecule in the blood of control rats. However, the fractional catabolic rate of α-1-antitrypsin from either well-nourished or protein-deficient rats was significantly (P < 0.01) lower in protein- deficient rats than in control rats (0.0247/h v. 0.0406/h).

5. The decreased fractional catabolic rate could not be explained by changes in hepatic mannosyl-, galactosyl- or N-acetylhexosaminyl receptors since liver perfusion studies showed that bovine serum albumin, when covalently modified separately with each of these ligands, was extracted from the perfusion medium as rapidly or more rapidly by livers from malnourished animals.

6. Perfused livers from protein-deficient rats secrete three times more α-1-antitrypsin than do livers from well-nourished animals.

7. The decreased fractional catabolic rate and increased rate of biosynthesis and secretion of the glycoprotein by livers from protein-deficient animals may account for the maintenance of α-1-antitrypsin levels during protein malnutrition.

1. Over- or undernutrition of newborn mice was caused by suckling in litters consisting initially of four or eighteen pups. After weaning, mice were fed ad lib. At 13 weeks some mice received gold thioglucose (GTG, 600 mg/kg, intraperitoneally) to induce hyperphagia, and all were killed at 39 weeks.

2. Mice suckled in small litters were heavier, with more body fat and protein. GTG treatment induced rapid weight gain and treated mice from large litters were heavier than untreated mice from small litters. However, the effect of litter size was not totally removed since GTG-treated small-litter mice were heavier than GTG-treated large-litter mice and had more fat, although body protein was not different.

3. Fat distribution between the depots was related to total body fatness and not to the treatment.

4. In male mice, preweaning undernutrition resulted in smaller fat depots containing smaller cells. GTG treatment of large-litter mice restored both to the levels found in small-litter mice: the depots of the latter mice were not significantly different after treatment.

5. In female mice, preweaning undernutrition resulted not only in smaller depots and cells but also fewer cells in all depots except mesenteric. GTG-treatment caused larger depots and cells in all mice with no difference in cell size whether mice were from large or small litters. The number of cells in the perirenal and mesenteric depots was greater in GTG-treated mice and was the same whether mice were from large or small litters.

6. We conclude that the level of preweaning nutrition does not affect the ability of adipose tissue to develop subsequently through hypertrophy or hyperplasia of the adipocytes or both, given a sufficient energy surplus consisting of normal pelleted feed, low in lipid.

1. The effects of a 100 g/kg diet substitution of bagasse on the body-weight gain, food consumption and faecal dry weight of mice given a high-sucrose diet and on the activities of hepatic glucose-6-phosphate dehydrogenase (EC 1. 1. 1. 49), 6-phosphogluconate dehydrogenase (EC I. I. I. 44), malate dehydrogenase (oxaloacetatedecarboxylating) (NADP+) (EC I. I. I. 40), ATP-citrate (pro-3S) lyase (EC 4. 1. 3.8), 6-phosphofructokinase (EC 2. 7. 1. II), pyruvate kinase (EC 2.7. 1. 40) and fructose-1,6-bisphosphatase (EC 3. 1. 3. II) were studied.

2. Bagasse had no effect on body-weight gain, food consumption or faecal dry weight.

3. Bagasse decreased the activities of glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase and phosphofructokinase expressed on a wet weight basis and on a protein basis.

4. Bagasse decreased the activities of glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydro-genase expressed on a body-weight basis.

5. These results suggest that bagasse decreases the flux through some pathways of hepatic lipogenesis when mice are given high-sucrose diets.

1. Studies of whole-body balances of non-metabolizable base (NB) and several minerals, and of relevant acid-base quantities in blood and urine, were carried out in two 6-month-old ruminating Holstein × Friesian bull calves fed on fixed rations containing 500 g barley straw/kg diet (group A) to examine the quantitatively important components of the balance of NB and determine the rates of mineral and NB retention associated with normal body growth.

2. Parallel balance studies were conducted in six other bull calves given fixed rations containing 500 g alkali-treated barley straw/kg diet to evaluate the effects of long-term alkali-straw feeding on the rates of body growth and skeletal mineral and NB deposition and the renal control of extracellular electrolyte and acid-base status. The straw component was treated either with 50 g sodium hydroxide/kg dry matter (DM) (group B; two calves), or with 50 g or 100 g NaOH/kg DM and subsequently neutralized with hydrochloric acid (groups C and D; two calves per group). In all groups the animals were given free access to tap water.

3. Throughout the total 105 d experiment, all animals remained healthy and gained weight. Normal body growth (group A) was associated with a positive balance of NB (1–2 mmol/kg live weight (LW) per d) due to continuing deposition of dietary NB in ‘new tissue’, largely in the developing skeleton.

4. During 105 d alkali-straw feeding, the animals showed a remarkable ability to cope with dietary loads of NaOH or sodium chloride, up to about 30 mmol/kg LW per d, without any significant disturbance of extracellular acid-base and electrolyte status or body growth rate. The surplus mineral and NB loads were absorbed and subsequently excreted in an increased volume of urine. Rates of mineral and NB retention were not significantly different from the reference values of group A and remained within the range of values reported from similar studies. In all groups, maintenance of normal whole blood and plasma acid-base and electrolyte status was accounted for by efficient renal control of the composition of the extracellular fluid compartment.

1. Thirty-three male, weanling guinea-pigs were divided into two groups. One group was fed on a zinc-deficient (ZnD) diet (1.25 mg Zn/kg diet) for 45 d and then divided into two subgroups: subgroup 1 continued on diet ZnD while subgroup 2 was fed on a Zn-repleted diet (100 mg Zn/kg diet) for 15 d. The second group was fed on a Zn-adequate diet (50 mg Zn/kg diet) for 60 d.

2. Zn deficiency could be produced within 21 d as evidenced by clinical signs and reduction in serum Zn concentration.

3. Clinical signs exhibited were listlessness, scabby lesions on skin near the foot pads, mild alopecia and a reduction in body-weight gain. No effect was observed on food intake.

4. Significant decreases in packed cell volume and total leucocyte count from 48 d onwards accompanied by absolute lymphocytopenia and relative neutrophilia were observed.

5. Supplementation of Zn in the Zn-repleted group resulted in marked, though incomplete, improvement with regard to serum Zn concentration, clinical signs and haematological changes.

1. Iron retention from 3 g wholewheat flour was measured in male Wistar rats previously given one high-Fe or control diet meal 12,24, 36,48 or 60 h before the test meal (Expt 1). The control diet was given at all other times. The procedure was then repeated in rats given one high- or low-Fe meal 12, 24, 36 or 48 h before the test meal (Expt 2).

2. There was a significant difference between groups given a high- or medium-Fe meal at 12,24,36 h (P < 0.001) and 48 h (P < 0.05) but not at 60 h. In the second experiment, there was a significant difference between groups given a high- or low-Fe meal at 12, 24 or 36 h but no difference when given the two diets 48 h before the test meal. The high-Fe meal depressed and the low-Fe meal enhanced subsequent 59Fe retention: the effects were greatest at 12 h and diminished as the time interval between the high- or low-Fe meal and the test meal increased. The estimated mean time for the absorptive capacity of the mucosal cells to return to equilibrium was 54.0 (SEM 7.6) h.

3. Male Wistar rats were given high-, control or low-Fe diets for either 3 d or 28 d before an in vivo investigation in which the luminal loss of 59Fe-labelled ferric citrate from duodenal and ileal loops was measured, and the proportional distribution between the carcass and the washed loop measured (Expt 3).

4. The luminal loss of 59Fe-labelled ferric citrate was significantly affected by the previous diets (P < 0.001). Rats given a low-Fe diet absorbed more than those given a high-Fe diet but the period of time on the diet (3 or 28 d) had no effect on luminal loss. Significantly more 59Fe was lost from duodenal than from ileal loops in all groups.

1. The cell-wall material of white lupin (Lupinus albus L.) cotyledon is characterized by low contents of cellulose (47 g/kg) and lignin (17 g/kg) and a high content of pectic substances (710 g/kg). The digestion of lupin cell-wall material by adult cockerels was estimated using gas-liquid chromatographic analyses of alditol acetates derived from polysaccharide sugars. The analyses were performed in the destarched water-insoluble fractions of feed and excreta. Digestibility measurements were carried out using a 3 d balance period including a 2 d feeding period and a 24 h final starvation period.

2. In the first experiment, six animals were given a diet containing 510 g white lupin cotyledon flour/kg which was the only source of protein and cell walls in the diet. The apparent digestibility of cell-wall components was near zero.

3. In the second experiment, three diets were prepared by diluting a fibre-free basal diet (diet A) by a semi-purified cell-wall preparation introduced at two different levels: 100 g/kg (diet B) and 200 g/kg (diet C). The semi-purified cell walls were prepared from the white lupin cotyledon flour used in the first experiment. The true digestibilities of polysaccharides measured in birds given diets B and C were near zero. It is suggested that the measurement of the neutral-detergent fibre (NDF) content according to Van Soest & Wine (1967) is not a suitable procedure for estimating the undigestible fibre content in poultry nutrition as the cell-wall pectic substances are not included in the NDF measurement.

4. Addition of the semi-purified cell-wall preparation (Expt 2) resulted in a slight decrease in the apparent protein digestibility. This decrease might be explained by the addition of undigestible cell-wall protein.

5. Addition of the semi-purified cell-wall preparation (Expt 2) had no effect on the apparent lipid digestibility.

6. The metabolizable energy values of the basal diet fraction of diets B and C were calculated assuming that the added plant cell-wall fraction was of no energy value. These calculated values were similar to the measured metabolizable energy value of diet A (basal). Thus, the tested pectic plant cell walls seemed to act as a diluent. It is suggested that, on the point of the digestion yields, all types of plant cell walls would act as diluents, in poultry.

1. The role of bacterial, dietary and intestinal phytases (EC 3. 1. 3. 8) in the hydrolysis of phytate was investigated in the golden hamster and rat by assaying phytase in the small intestine and by measuring the disappearance of phytate from the stomach and large intestine, using chromium oxide as an insoluble solid-phase marker.

2. It was confirmed that an active phytase was present in the proximal third of the small intestine of the rat but the enzyme was undetectable in the hamster.

3. Extensive bacterial breakdown of phytate occurred in the pregastric pouch and true stomach of the hamster with both phytase-containing and phytase-free diets, with phytate digestibilities in the true stomach ranging from 0.69–0.90, confirming that the hamster can be regarded as a pseudo-ruminant.

4. With a phytase-free diet, the digestibility of phytate in the stomach of the rat was very low (0.05) but with a wheat-based diet substantial breakdown of phytate occurred (digestibility up to 0.49), presumably under the influence of the cereal phytase.

5. Intestinal phytase did not appear to be of great significance in the rat but some further hydrolysis of the residual phytate probably occurred in the large intestine of both species by bacterial phytase.

1. To characterize the hypercholesterolaemic effect of casein further, four groups of young male rabbits in two separate experiments were placed on cholesterol-free semi-purified diets for 12 weeks. The diets were similar in composition, with either casein or soya-bean-protein isolate providing the protein source (250 g/kg). In two of these diets the salt mix was reduced by 45% (normally 40 g/kg) and replaced by potassium bicarbonate.

2. Growth was unaffected by these alterations in dietary salts except for one group given the soya-bean-reduced-salts diet.

3. The mean concentrations of plasma cholesterol were significantly higher in all casein-fed groups as compared with their soya-bean-fed counterparts but the response was much greater in those given the casein—reduced-salts diet.

4. Contrary to expectations, analysis of the diets showed the zinc and copper concentrations of the casein diets to be less than those of the soya-bean diets. This was due to the greater concentrations of Cu (threefold) and Zn (twofold) in the soya-bean-protein isolate compared with casein.

5. The mean concentration of Zn in fur was significantly decreased in casein-fed rabbits and these animals also excreted less Zn but more Cu in their urine than those given the casein—reduced-salts diet.

6. The rabbits given the casein diet with the least salt mix showed the greatest degree of hypercholesterolaemia, suggesting an interaction between trace elements and the casein effect.

1. Inclusion of raw kidney bean (Phasealus vulgaris) proteins in the diet for rats was shown to affect the weight of some internal organs. Of these, in addition to the well-known hypertrophy of the pancreas attributable to dietary trypsin inhibitors, the observed atrophy of the thymus and the doubling in weight of the small intestine are related to the protein or lectin content of the bean diet, or both.

2. Changes in tissue composition of the small intestine were also recorded. Its protein content increased by about 40–50% and carbohydrate content doubled suggesting the occurrence of increased mucinous glycoprotein secretion. Increased DNA content (by about 30–40 %) however also indicated mucosal hyperplasia.

3. Changes were also observed in mineral content, urea concentration and some enzyme activities in sera and urine, possibly as a result of disturbances in systemic metabolism or hormone levels, or both.

4. The results gave further support to previous suggestions that the oral toxicity of kidney-bean lectins involves local reactions in the small intestine in combination with their effects on the systemic immune system and general metabolism.

1. The effects on growth performance, energy and nitrogen retention, and leucine metabolism of a subcutaneous combined implant of 140 mg trenbolone acetate (TBA)+20 mg oestradiol-17β (OE) have been examined in Hereford × Friesian beef steers (280–520 kg). Comparisons were made both with the same animals before implantation and with untreated control animals maintained under similar physiological and nutritional conditions.

2. Over a 10 week period the implanted steers showed an improvement in rate of live-weight gain (LWG) of 0.5–0.6 with an even greater proportional increase in N retention compared with control animals. Total energy retention was unaffected and thus the ratio, protein energy: total energy gain was 0.43 for implanted steers compared with 0.26 for untreated animals.

3. Estimates of protein synthesis and protein oxidation were obtained from the specific radioactivities of blood free-leucine and exhaled carbon dioxide during continuous infusions of [1-14C]leucine. Whole-body protein synthesis, based on metabolic size, and amino acid fractional oxidation remained similar for control steers throughout the experiment. Steroid-treated steers showed a slight decline in synthesis which was significant (P < 0.05) at week + 5 post-implant while amino acid oxidation was significantly lower at weeks +2 (P < 0.01) and + 5 (P < 0.05) compared with control animals. The ratio, protein deposition: protein synthesis was 0.05 for control animals but 0.08–0.10 for steroid-treated animals after implantation.

4. There was a slight decrease in urinary NT-methylhistidine elimination after implantation which suggested that muscle protein degradation may be reduced although the estimated decrease was insufficient to account for the total improvement in growth rate and N retention.

5. The results suggest that for both control and treated steers, less than 0.5 of total urine N elimination was derived directly from tissue catabolism of protein and amino acids.

6. The combined action of the exogenous steroids in the promotion of protein gain, primarily through a decrease in total protein degradation with little alteration of total energy retention, is compared with present understanding of the role of the endogenous sex hormones.

1. A technique for measuring gastric emptying in growing pigs by complete removal of digesta through a gastric cannula is described.

2. Four pigs were fitted with gastric cannulas and each was used in three trials.

3. The effects of level of feeding (trial 1), cellulose (C), maize-oil (MO) or sucrose (SU) supplementation (trial 2) and the level of water intake (trial 3) on gastric emptying of digesta, dry matter (DM) and nitrogen from a barley-weatings-soya-bean (B) diet were measured during 4 h after the morning feed.

4. In trial 1, pigs were given 0.66, 0.83, 1. 00 or 1. 17 times their standard level of feeding. As the level of feeding rose, so the weight of digesta, DM and N emptied in the first hour after feeding increased. This trend continued to some extent in the second hour, but no effects of level of feeding were seen in the third and fourth hours.

5. In trial 2, maize-oil addition to the diet significantly reduced the gastric-emptying rate of DM in the second hour after feeding, compared with the rates for diet C. The rate of N emptying was significantly slower for diets MO and SU than for diet C.

6. In trial 3 there were no significant effects of water intake level (1. 75, 2. 50 and 3. 25 times the weight of diet) on the rate of DM or N emptying from the stomach. The rate of digesta (and thus of water) emptying in the first hour after feeding increased significantly as the water intake rose.

7. It was concluded that because the pattern of gastric emptying was very similar despite large differences in nutritional inputs, an important property of the process appeared to be resilience.

1. To elucidate the causal relation between leucine and the lowering of hepatic NAD content of rats fed on a leucine-excessive diet (Yamada et al. 1979), the effect of leucine on intestinal absorption of tryptophan was investigated.

2. Co-administration of [3H]tryptophan and leucine, with leucine at ten times the level of tryptophan, delayed absorption of L-[side chain 2,3-3H]tryptophan from the digestive tract and incorporation of [3H]tryptophan into portal blood, the liver and a protein fraction of the liver. After 120 min, more than 95% of tryptophan was absorbed whether [3H]tryptophan was administered with or without leucine.

3. Co-administration of a mixture of ten essential amino acids, in proportions simulating casein, with [3H]tryptophan markedly delayed absorption of tryptophan from the digestive tract. The addition of supplementary leucine to the amino acid mixture, however, caused no further delay.

4. In rats prefed a leucine-excessive diet for 1 week [3H]tryptophan was absorbed at the same rate as in rats fed on a control diet.

5. The results indicate that competition between tryptophan and leucine for intestinal absorption did not cause lowering of hepatic NAD.