1. The degree to which disruption by mastication affects the glycaemic response to four different carbohydrate foods was investigated in healthy human volunteers; each food was eaten by six subjects.

2. Subjects ate meals of sweetcorn, white rice, diced apple or potato on two occasions; on one occasion they chewed the food thoroughly, on the other occasion they swallowed each mouthful without chewing it.

3. When the foods were chewed the postprandial blood glucose levels rose to levels which vaned according to the food ingested.

4. Swallowing without chewing reduced the glycaemic response to each food, achieving a similar effect as administration of viscous polysaccharides or ‘slow-release’ carbohydrates.

1. To examine the relations between short- and long-term regulation of food intake in calves given milk-substitute diets, abrupt changes were made in the dry matter (DM) concentration of the diet (Expt 1) and in the frequency of feeding (Expts 2 and 3).

2. When calves, fed once daily, had the DM concentration of their diet changed, they drank the same volume of milk on the 1st day they received the new diet as they had on the previous days; so the DM intakes changed in proportion to the change in milk DM concentration. Over the subsequent 6 d, milk intake progressively increased when milk DM concentration was reduced. When the DM concentration of milk was increased the volume of milk drunk was reduced to a minimum value 2–3 d after the change in diet and increased thereafter. The size of the changes was dependent on the initial and changed DM concentrations of the milk.

3. In calves receiving milk-substitute diets containing 80–260 g DM/kg, milk intakes were reduced by up to 30% on the 1st day that calves were fed once daily instead of twice daily. Over the subsequent 13 d of once-daily feeding, milk intakes increased, particularly for calves given diets of low DM concentration.

4. Feeding the calves once daily reduced the digestibility of DM in Expt 2 but not the digestibility of crude protein (nitrogen × 6.25) and fat; diets containing lower concentrations of DM were particularly affected.

5. It is concluded that the intake of milk-fed calves at a single meal is regulated by an abomasal stretch mechanism. After an abrupt change in milk DM concentration or in the frequency of feeding, the amount of milk drunk at subsequent meals is modified by some long-term control mechanisms.

1. Very little is known about the biological availability of manganese from human milk and other infant milk diets. To determine the relative Mn availability, and to examine whether the age and the duration of previous fasting affect Mn absorption, sucking rats were given human milk, bovine milk and infant formula (regular Similac; Ross Laboratories, Columbus, OH) extrinsically labelled with 54Mn.

2. Milk diets were given by gastric intubation and the radioactivity of the carcass, liver and digestive tract was measured 3 h after feeding.

3. The concentration of endogenous Mn was lowest in human milk (7–10 μg/l) and highest in rat milk (140–165 μg/l). Increasing the non-radioactive total Mn concentrations of either human milk or bovine milk up to 150 μg/l did not affect the absorption of 54Mn by 10-d-old rats.

4. No significant (P> 0.05) difference in 54Mn absorption was found among the three milk diets (human milk, bovine milk, infant formula) in 8- to 11-d-old rats. However, significantly more (P< 0.05) 54Mn was absorbed from human milk and infant formula than from bovine milk when 13-d-old rats were used.

5. 54Mn radioactivity detected in carcasses of 8-, 9-, 10- and 11-d-old rats ranged from 25 to 27% of the dose from various milk diets. The activities of 54Mn in the carcasses of 13-d-old rats were 15, 11, and 16% of the dose from human milk, bovine milk and infant formula respectively.

6. The trend of 54Mn incorporation into liver was similar to that of the carcass and over 60% of the absorbed 54Mn was incorporated into the liver regardless of the type of milk used.

7. Absorption of 54Mn from extrinsically labelled rat milk using 9- or 10-d-old sucking rats was similar to its absorption from infant formula.

8. The absorption of 54Mn from the three milk diets decreased with age of the neonatal rats and 54Mn absorption from human milk, bovine milk, infant formula as well as rat milk was affected similarly by duration of previous fasting.

1. During 1978 and 1979, the 343 members of seventy-nine families representative of households with two adults and two or three children living in Cambridge, England, completed 7-d records of food consumption using the semi-weighed technique. Nutrient intakes were calculated using food composition tables.

2. Amongst males, the average intakes of energy and most nutrients were highest in men and boys aged 11–17 years, and lowest in boys under 5 years. Amongst females, intakes were highest in girls aged 11–17 years, and lowest in those under 5 years. At each age, intakes in males were generally higher than those in females.

3. Nutrient distribution within families was described using the ratio, intake of each subject: intake of the male head of the household. The problems inherent in using this ratio are discussed.

4. The distribution of nutrient intakes within the families was not in accordance with the recommended daily amounts (RDA). Men and young boys received more than their fair share of the family diet, while women and girls aged 5–17 years received less.

5. Estimates of dietary adequacy based on the averages of family consumption and requirements (RDA) concealed up to twofold variations in the adequacy of diet of different age-sex-groups.

6. The interpretation of dietary adequacy in household food surveys should take into account the distribution of nutrient intakes within the household, as the distribution may be substantially different from that predicted by the RDA.

1. Iron absorption from 10 mg Fe (as ferrous sulphate), labelled with 1.3 mg 58Fe, was measured in fasting, non-anaemic adult subjects by the faecal-balance technique. The measurement was performed twice, each subject being given, in random order, either 50 mg Fe or a placebo 18 h before the 58Fe-labelled FeSO4.

2. The 50 mg Fe load significantly reduced Fe absorption the following day (P < 0.01), from a mean of 35.4 (SEM 4.6)% to 29.0 (SEM 5.1)%. This points to the importance of strict dietary control during Fe-absorption studies to eliminate bias in results.

3. In a separate study, the feasibility of using S6Fe-enrichment of erythrocytes, measured by neutron activation analysis (NAA), 10 d after a meal labelled with 0.69 mg 58Fe as an index of Fe absorption was examined. The levels of 58Fe in the blood were detectable by NAA. Regression analysis showed a significant relation between 58Fe-enrichment of blood and 58Fe absorption, calculated as the difference between intake and faecal excretion (R 0.59, P < 0.05).

1. Four cows in early lactation were given continuous infusion into the abomasum of 0, 200, 400 or 600 g lactic casein/d according to a Latin-square design. Each period was of 14 d and the Latin square was followed by 7 d in which an infusion of 800 g glucose/d was given. The basal diet was given at a level which provided sufficient nitrogen and energy for 10 kg milk yield/d.

2. Infusion of casein resulted in significant increases in milk yield, milk N yield and milk energy yield; milk N increased progressively but milk energy reached a maximum at 400 g casein/d. Milk yields and composition when glucose was infused resembled those seen on the zero casein treatment.

3. N-balance measurements indicated a severe deficit (–20 g/d) on the zero casein treatment and a progressive increase to +7 g/d as casein increased; N equilibrium was achieved at about 400 g casein/d. The regression of net productive N on N intake (P < 0.001) indicated that the efficiency of utilization of dietary N did not differ between treatments.

4. Heat production increased with increase in casein infused (P < 0.05) but remained a constant proportion of the metabolizable energy (ME) intake. Energy balances were negative and did not differ significantly between treatments but calculation of the protein and fat components indicated a threefold increase in body fat mobilization in response to the first increment of casein. Milk yield adjusted to zero energy balance was significantly related to ME intake (P < 0.001) but the efficiency of encrgy utilization was not affected by the level of casein infusion.

5. The concentrations of glucose, β-hydroxybutyrate and non-esterified fatty acids in plasma did not differ between treatments but the concentration of urea in plasma increased markedly (P < 0.05) at the highest level of casein addition. Insulin concentrations increased and growth hormone decreased (both P < 0.05) with increase in casein infusion.

6. The concentration of total amino acids (AA) in plasma increased up to 400 g casein/d and then declined. Changes in concentration and in the ratio of essential: total AA indicated a very high extraction rate of essential AA at the lower levels of casein infusion.

7. The observed lactational responses are discussed in relation to the ratio of protein:energy in the absorbed nutrients. It is concluded that the primary response to casein was the correction of an AA deficit and that body fat mobilization was secondary and occurred in response to the high ratio of AA-N:energy in the infused casein.

1. It has been suggested that zinc-deficiency impairs cellular (T-lymphocyte-mediated) immune responses via a selective effect on helper T-lymphocytes. We have addressed this question in the rat by employing recently developed reagents in the form of monoclonal antibodies which specifically identify rat T-lymphocyte subsets (identifying total T-cells, helper T-cells and suppressor T-cells) and also by quantifying helper T-cell function by measurement of the helper T-cell-derived molecule interleukin-2 (IL-2).

2. Zn-deficiency induced T-cell atrophy (assessed morphologically and phenotypically with anti-rat T-cell monoclonal antibodies) in both peripheral blood and spleen. The use of these specific monoclonal antibodies failed to demonstrate a selective effect of Zn deficiency on the helper T-cell fraction of the total T-lymphocyte population.

3. In contrast, the results of functional assays of the T-lymphocyte response were dependent on the conditions of culture but suggested that the generation of IL-2 and its corresponding receptor were determined by the intracellular Zn status. Thus, in vivo, helper T-lymphocyte numbers are non-specifically reduced since other T-cell subsets are also reduced in response to appropriate stimulation. The functional consequences of this are dependent on the intracellular concentration of Zn but appear to influence both IL-2 production and its receptors on activated T-cells.

1. Alkali (sodium hydroxide)-treated wheat straw was given to six rumen- and abomasal-cannulated sheep to study the rumen degradation of cotton-seed meal (CSM) and barley (B), and the effects of these supplements on nitrogen retention and efficiency of bacterial protein synthesis were measured.

2. N degradation, using porous synthetic (nylon) bags incubated within the rumen (P), and in vivo measurement determined from the abomasal flow of N (V), distinguished quantitatively between the two supplements. Estimates of P, corrected for fractional outflow rates/h (FOR), underestimated estimates of V when FOR of undegraded protein from the rumen (k) of 0.05 and 0.08 were used. Estimates of V for CSM and B were 70.9 and 80.8% respectively.

3. Intakes of alkali-treated straw were not affected by the supplements. Intakes of digestible organic matter (DOM) for the diets comprising alkali-treated straw alone (W), straw plus CSM (WC) and straw plus barley (WB) were 477, 575 and 590 g/d respectively (P < 0.05) and organic matter (OM) apparently digested in the rumen (OMADR) was 339, 399 and 435 g/d respectively (P < 0.05).

4. On W, WC and WB respectively, flows at the abomasum were 11.0, 14.0 and 13.3 g/d for bacterial N (P < 0.05) and 0,2.8 and 0.5 g/d for dietary supplemental N; g bacterial N/kg OMADR were 32.4, 35.6 and 30.9 (P > 0.05) and N balances were 2.37, 4.27 and 3.29 g/d (P < 0.05) on the respective treatments. It was suggested that supplements increased total OM intake as a result of increased OM digested in the rumen rather than OM flow from the rumen.

1. In a randomized, double-blind 6-month study, α-tocopherol (728 mg) or placebo were administered daily to seventy-eight volunteers (forty-nine men, twenty-nine women) to investigate the possible enhancing effect of vitamin E on plasma high-density-lipoprotein-cholesterol (HDL-C) levels. In addition, the available reported values from short-term (4–6 weeks) studies, as well as the 4-week results from the present study, were combined and analysed for factors which may modify the effect of α-tocopherol on HDL-C.

2. No consistent effect of α-tocopherol on plasma HDL-C levels was observed either in the combined 4-week values or in the 6-month study. Further analysis of the combined short-term values and 6-month values indicated that, in subjects with low initial HDL-C levels, treatment with α-tocopherol or placebo did not produce significantly different HDL-C changes.

1. The effects of a 100 g/kg dietary substitution of wheat bran on the body-weight gain, food consumption and faecal dry weight of mice given a high-sucrose diet and on the activities of some key enzymes of carbohydrate and lipid metabolism in liver and adipose tissue were studied.

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

3. Wheat bran had no effect on the activities of hepatic glucose-6-phosphate dehydrogenase (EC 1.1.1.49), 6-phosphogluconate dehydrogenase (EC 1. 1.1.44), malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+) (EC 1. 1. 1.40), ATP-citrate (pro-3S)-lyase (EC 4.1.3.8), pyruvate kinase (EC 2.7.1.40) and fructose-1, 6-bisphosphatase (EC 3.1.3.11). The activity of hepatic 6-phosphofructokinase (EC 2.7.1.11) increased but only when expressed on a body-weight basis.

4. Wheat bran had no effect on the activities of adipose tissue glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, malate dehydrogenase (oxaloacetate-decarboxylating) (NADP+), (ATP-citrate igro-3S)-lyase, hexokinase (EC 2. 7. 1. 1), 6-phosphofructokinase and pyruvate kinase.

5. These results suggest that unlike guar gum and bagasse, wheat bran does not change the flux through some pathways of lipogenesis in liver and adipose tissue when mice are given high-sucrose diets.

1. The effect of cholesterol feeding during and after a period of protein malnutrition lasting 4 weeks was examined in the rat. Indices measured were plasma total cholesterol, triglycerides and protein levels, and aorta total cholesterol, triglycerides, hexosamine and hydroxyproline concentrations.

2. In both plasma and aorta, total cholesterol and triglycerides levels were higher in the low-protein diet group than in the standard-protein diet group, when cholesterol was supplied in both diets.

3. During the malnutrition period, cholesterol feeding led to a greater decrease in plasma protein than that promoted by the low-protein diet without cholesterol, while aorta hexosamine levels decreased to a lesser extent.

4. Cholesterol feeding with a standard-protein diet promoted a slight and temporary increase in aorta hydroxyproline levels, while a decrease in aorta hexosamine concentration was observed. Cholesterol feeding with the low-protein diet, on the other hand, also promoted a decrease in aorta hexosamine levels but to a lesser extent.

5. During the recovery period, cholesterol feeding impaired the return of plasma protein, aorta hexosamine and lipid levels to that of the control values.

6. These findings demonstrate that cholesterol feeding promotes different changes in aorta and plasma, depending on whether or not protein is supplied by the diet in adequate amounts. This point could be important in relation to the development of atherosclerosis during recovery from a period of malnutrition.

1. Two studies were performed to determine the effects of acid stress and ovariectomy on bone metabolism in young rats. In Expt 1, eighteen female weanling Sprague-Dawley-descended rats were ovariectomized, placed in one of three dietary groups and given a diet containing (g/kg): 6 calcium and 3, 6 or 12 phosphorus for 10 weeks. In Expt 2, thirty-two female weanling Sprague-Dawley-descended rats were ovariectomized, and thirty-two were left intact. Eight rats from each group were given a diet containing (g/kg): 6 Ca and 3 P, 12 P, 3 P+1 S or 3 P+20 ammonium chloride for 10 weeks.

2. Feeding diets containing 12 g P/kg resulted in decreased serum Ca and increased urinary P with no changes in femur composition. Feeding high-sulphate and ammonium chloride diets resulted in increased urinary Ca and, when combined with ovariectomy, lower femur Ca and P with no changes in femur hydroxyproline or hexosamines.

3. The findings reflect the more rapid turnover of the amorphous calcium phosphate salts found in greater amounts in bones of younger animals than for more stable apatitic crystals that predominate in bones of older animals.

1. Digesta were collected from eleven preruminant calves fitted with re-entrant (four calves in Expt 1 and three in Expt 2) or single cannulas (four calves in Expt 1) in the terminal ileum. Collection periods lasted 24 h (Expt 1) or 96 h (Expt 2).

2. Two milk-substitutes (fish and soya bean) and a control diet were given to the calves. In the control diet, protein was entirely provided by skim-milk powder. In the other two diets, protein was provided mainly by a partially hydrolysed white-fish protein concentrate or a soya-bean protein concentrate prepared by extracting soya-bean meal with hot aqueous ethanol.

3. In Expt 1, flow rates of fresh matter, dry matter, nitrogen and ash exhibited two maxima between 6 and 8 h after the morning meal and between 4 and 6 h (control and soya-bean diets) or 6 and 8 h (fish diet) after the evening meal. Minimum pH values were observed at times of maximum flow rate. Variations observed in the flow rates and pH values were larger with fish and especially soya-bean diets than with the control diet.

4. The apparent digestibility of the three diets in the terminal ileum was significantly higher in Expt 2 than in Expt 1: for N, the values were 0.92, 0.83 and 0.75 (Expt l), and 0.94, 0.87 and 0.88 (Expt 2) with the control, fish and soya-bean diets respectively.

5. The amount of N apparently absorbed in the terminal ileum represented 90–96% of the amount that disappeared from the whole digestive tract in Expt 1 and 95–99% in Expt 2.

6. In Expt 1 the amino acid (AA) composition of digesta changed little with the flow rate when the calves were given the control diet (from 158 to 179 g glutamic acid/kg AA). With the fish and soya-bean diets the AA composition was similar to that observed with the control diet when the flow rate was minimum, but differences became apparent as the flow rate increased (281 and 161 g glutamic acid/kg AA for the soya-bean and control diets respectively with maximum flow rate). In Expt 2, the mean compositions of the digesta were very similar to the means obtained in Expt 1.

7. Different comparisons with dietary, endogenous and bacterial proteins indicated that for the three diets a common mixture containing approximately 65% endogenous and 35 % bacterial proteins reached the terminal ileum. The quantity of dietary protein added to this mixture appeared to be very low with the control diet, but it increased with the flow rate in the case of the fish and soya-bean diets.

8. In Expt 2, the additional undigested protein in the small intestine was richer in glycine with the fish diet and in glutamic acid and aspartic acid with the soya-bean diet compared with the control diet. This undigested fraction probably originated mainly from the fish solubles and the glycinin of soya bean respectively.

9. With the control diet the apparent digestibility of threonine and cystine was always lower than the mean value for all AA while that of methionine was higher (0.92, 0.82 and 0.96 respectively). Digestibility of all AA was higher for the control diet than corresponding values for the fish and soya-bean diets; these differences were greatest for histidine with the fish diet (–0.11) and for glutamic acid with the soya-bean diet (–0.13).

1. Simple gastric cannulas were surgically fitted to four pigs, initially of 30 kg live weight, to examine the effects of guar gum on gastric emptying.

2. Four semi-purified high-fat diets based on starch, casein, soya-bean oil and tallow were given to each pig. They contained 0 (control), 20, 40 or 60 g powdered guar gum/kg diet. The meals as fed contained 257 g dry matter (DM)/kg.

3. The contents of the stomach were evacuated, with rinsing, before feeding or 0.5, 1, 2 or 4 h after feeding.

4. The mean pH of the digesta was unaffected by guar gum until 4 h after feeding when the value increased as the amount of guar gum in the diet rose.

5. The only significant effects of guar gum on the emptying of digesta and its components (compared with the control diet) were to reduce the rate of emptying of (a) digesta 1 h after feeding (60 g/kg diet) and 4 h after feeding (40 and 60 g/kg diets), (b) dry matter and glucose 1 h after feeding (60 g/kg diet), (c) nitrogen 1 h after feeding (60 g/kg diet) and 4 h after feeding (40 and 60 g/kg diets).

6. When expressed on a half-time (T50) basis, the emptying of digesta and N (but not of DM and glucose) were significantly slower for diets containing 40 and 60 g guar gum/kg than for the control diet.

7. The apparent viscosity of the gastric digesta ranged between 0.5 and 23.7% of the values for the diets as consumed.

8. It was concluded that the effects of guar gum on gastric emptying of high-solid meals were small, and that this was unlikely to be an important aspect of the mechanism by which guar gum reduces postprandial blood glucose concentrations.

1. Ten 5-month-old lambs (29 (SE 1.2) kg), reared parasite-free and prepared with rumen duodenal and ileal cannulas, were paired and given rations of Ruminant Diet AA6 (90 g/kg live Weight0.75) by means of continuous feeders. From 6 months of age one of each pair was dosed daily with 2500 Trichostrongylus colubriformis larvae for 14 weeks. Untreated animals received the amount of ration consumed by their infected pair-mates the previous day.

2. During three periods, ((1) the week before and the first 2 weeks of dosing with infected larvae, (2) during weeks 5–7 and (3) during weeks 11–13 of dosing) all lambs underwent a series of experiments to determine their nitrogen balance, the amounts of N leaving the small intestine, the amount of 51CrC13-labelled plasma protein leaking into the small intestines, and the disappearance of 35S-labelled bacteria from the small intestine.

3. The infection caused varying degrees of feed refusal in all infected animals. As a result the values for N balance and for the flow of N at the ileum during the latter two periods were regressed against dry-matter intakes for each group in each period.

4. The infection caused a reduction (P < 0.05) in N retention and increased (P < 0.05) flow of N at the ileum. The increase in N flow at the ileum of infected lambs was greater (P < 0.01) at weeks 11–13 of dosing (infected–control 3.6 g N/d (standard error of difference (SED) 0.57), P < 0.01) than at weeks 5–7 of dosing (infected–control 1.5 g N/d (SED 0.57), P < 0.05).

5. There were no between-treatment or between-period differences in the disappearance of 35S-labelled bacteria from the small intestines of infected or control lambs, but the infection did cause an increase in plasma N leakage during both periods. During weeks 5–7 and 11–13, plasma N leakage in infected lambs was 1.1 g N/d (P < 0.01) and 1.7 g N/d (P = 0.056) respectively higher than that in the control lambs.

6. A proportion of the endogenous secretions which enter the small intestine is likely to be resorbed before the ileum. It was calculated that to account for the extra non-ammonia-N (NAN) flow at the ileum up to 3–5 g NAN/d during weeks 5–7 of dosing and 15–20 g N/d during weeks 11–13 of dosing could have entered the small intestine as mucin and sloughed cells.

7. The results seem to indicate that the nutritional penalty associated with the development of resistance to infection is greater than that associated with the primary infection.

1. Two duplicate groups of rainbow trout (Sulmo gairdneri; mean weight 27 g) were given diets of differing selenium content (deficient 0, 025 mg Se/kg; supplemented 1.022 mg Se/kg) for 30 weeks.

2. There were no significant differences between treatments in weight gain but packed cell volume, liver vitamin E and liver and plasma Se concentrations were all significantly lower in the Se-deficient trout.

3. Ataxia occurred in about 10% of the Se-deficient trout and histopathologies were evident in nerve cord (damage to axon sheath) and liver (loss of integrity in endoplasmic reticulum and mitochondria with appearance of increased vesiculation).

4. Glutathione peroxidase (EC 1.11.1.9) activity was significantly reduced in liver and plasma of Se-deficient fish but there was no indication, from differential assay, of any non-Se-dependent glutathione peroxidase activity. Glutathione transferase (EC 2.5. I.18) activity was significantly increased in Se-deficient trout.

1. Existing information on whether the action of guar gum in decreasing postprandial blood glucose concentrations is due, at least in part, to a reduced rate of gastric emptying is conflicting, possibly because three types of test meals have been used. In order to test whether the type of test meal used influences the action of guar gum, these three types of meal were compared, either without or with guar gum, in growing pigs. The meals were: a high-energy meal (HEM), a low-energy milky drink (LEMD) and a glucose drink (GD).

2. Six pigs were prepared with a simple gastric cannula which allowed complete removal of the stomach contents just before or 0.5, 1, 2 or 4 h after feeding.

3. The three types of test meal without guar gum gave rise to very different postprandial profiles of gastric pH and of digesta and dry matter (DM) emptying from the stomach.

4. Addition of guar gum to the GD significantly raised gastric pH at 0.5 and 1 h after feeding but, when it was added to HEM, gastric pH was only significantly raised 4 h after feeding. No significant effect on gastric pH was seen when guar gum was added to LEMD.

5. Although addition of guar gum to GD had no significant effect on the emptying of digesta from the stomach, when added to HEM the rate of emptying of digesta was significantly reduced 1, 2 and 4 h after feeding. Addition of guar gum to LEMD only significantly increased the amount of digesta remaining in the stomach 2 h after feeding.

6. There was no significant effect on the emptying of DM from the stomach when guar gum was added to either HEM or LEMD. However, addition of guar gum to GD significantly reduced the mean rate of emptying of DM 0.5 h after feeding.

7. Addition of guar gum to either LEMD or GD had no significant effect on the DM concentration of the evacuated gastric digesta. However, addition of guar gum to HEM significantly lowered the DM concentration of the evacuated gastric digesta 1, 2 and 4 h after feeding.

8. It was concluded that differences in test meal composition and also in the methods used to measure gastric emptying could account for the discrepancies previously reported. The results suggest that although guar gum may reduce the rate of gastric emptying under some conditions, this is unlikely to be the only mechanism by which it acts.

1. Experiments involving 15N and 14C tracers were made in sheep consuming 800 g air-dry chopped lucerne (Merlicugo sativa) hay/d and providing 20.4 g N/d to study N and C flows within the caecal digesta and between the caecum, blood and rumen.

2. Continuous infusions of 15N tracers were made into the caecal ammonia, blood urea and rumen NH3 pools. The concentration and enrichment of caecal digesta NH3-N, caecal microbial N, caecal digesta non-urea. non-ammonia-N (NU-NAN), faecal NU-NAN, blood urea-N, rumen digesta NH3-N and rumen bacterial N were estimated at intervals during the infusions. A three-pool open-compartment model was solved to estimate N flows between the caecal digesta NH3-N, blood urea-N and rumen digesta NH3-N pools.

3. The rate of irreversible loss from the caecal digesta NH3-N pool was 2.17 (SE 0.623) g N/d. On average 0.9 (SE 0.56) g N/d of caecal digesta NH3-N was derived from blood urea and 0.1 (SE 0.08) g caecal digesta NH3-N/d was apparently derived from the fermentation of undigested rumen microbes in the caecum. The amount of NH3-N produced by proteolysis and deamination of dietary and endogenous N was 1.1 (SE 0.13) g/d.

4. There was net incorporation of 0.56 (SE 0.306) g caecal digesta NH3-N/d into caecal microbes. The microbial U synthesized de novo in the caecum was not determined, but 2.9 (SE 0.52) g microbial N/d of both rumen and caecal origin flowed out of the caecum and constituted 0.48 of the NU-NAN flow. The majority (mean 0.83 (SE 0.044)) of this microbial N was excreted in faeces.

5. On average 1.8 (SE 0.80) g caecal digesta NH3-N/d were absorbed. Of this NH3-N, 0.92 (SE 0.054) was converted to blood urea, contributing 0.10 (SE 0.031) of blood urea-N. Only 0.012 (SE 0.0041) of rumen digesta NH3-N and 0.005 (SE 0, 0009) of rumen bacterial N were derived from caecal digesta NH3-N.

6. Infusions of 14C tracers were made into the caecal digesta bicarbonate, blood bicarbonate, rumen digesta bicarbonate and blood urea pools, and samples were obtained at intervals to determine the specific radioactivity of each pool. A four-pool open-compartment model was solved to estimate C flows between these pools.

7. The rate of irreversible loss of blood urea estimated with [14C]urea (17.1 (SE 1.18) g N/d) was greater (P < 0.01) than that estimated with [15N]urea (14.0 (SE 0.87) g N/d).

8. Transfer of blood urea to the caecal digesta estimated with 14C tracers (1.4 (SE 0.61) g N/d) was greater (P < 0.01) than that estimated with I5N tracers (0.9 (SE 0.56) g N/d). The estimate of transfer of blood urea to the rumen digesta was also greater with 14C tracers (P < 0.05; 1.7 (SE 0.15) and 1.2 (SE 0.19) g N/d respectively). The urea hydrolysed in the gastrointestinal tract other than in the rumen digesta pool and the caecal digesta pool was 0.56 of total urea hydrolysis when estimated with 14C tracers, or 0.69 when estimated with 15N tracers. Results from previous acute experiments suggested that with three of the four observations made in three sheep in the present experiment the transfer of blood urea to the caecal digesta could have occurred entirely via ileal digesta. Similarly, urea transfer to the rumen digesta could have occurred entirely via saliva.

1. Immature, male Wistar rats were given a low-zinc diet (2 mg/kg) for 22–24 d. Control groups received a similar diet supplemented with 58 mg Zn/kg either ad lib., or in amounts matched to the consumption of the Zn-deficient group. Food consumption, rate of growth and food conversion efficiency were markedly lower in the Zn-deficient group of rats compared with controls. Appetite, growth rate and food utilization improved dramatically over a subsequent 4 d period of Zn supplementation.

2. Morphological examination of samples of jejunum and ileum confirmed that Zn deficiency in the rat is accompanied by a reduction in villous dimensions and increase in villous density. After a short period of Zn supplementation, villous density and the basal width and maximum height of individual villi in the jejunum returned to normal. Similar changes occurred in the ileum but to a lesser extent.

3. Mucosal alkaline phosphatase (EC 3.1.3.1) activity was significantly lower in the small intestine of Zn-deficient rats compared with Zn-supplemented rats. Disaccharidase activities were lower in the Zn-deficient group, compared with their feed-restricted counterparts, but were similar to values for ad lib.-fed controls. Tissue alkaline phosphatase and disaccharidase activitities were consistently higher after a 4 d period of Zn supplementation, compared with non-supplemented animals, but this increase was only significant for alkaline phosphatase.

4. Although there were striking similarities in the mucosal characteristics of gnotobiotic and Zn-deficient rats, there was no indication that even severe dietary Zn depletion reduced the numbers of viable bacteria present in either the small or large intestine. Changes in intestinal structure and function resulting from variation in dietary Zn intake appear, therefore, to be unrelated to changes in the intestinal flora.

1. Five pigs initially of 40–50 kg live weight were fitted with simple gastric cannulas which permitted complete evacuation and sampling of gastric digesta once daily.

2. The effects of addition of four types of dietary fibre(wheat bran (WB; 40 g/kg), sodiumcarboxymethylcellulose (CMC; 40 g/kg), high-methoxy citrus pectin (Pe; 40 g/kg) and granulated guar gum (G; 40 g/kg)) on gastric emptying of a semi-purified diet during 4 h following a meal were measured.

3. Each of the test diets and the control diet (C) were given to each pig for 1 week using a 5 x 5 Latin-square arrangement. Digesta were collected before and 0.5, 1, 2 or 4 h after feeding on the last 5 d of each week.

4. The mean gastric pH was not significantly affected by diet except 2 h after feeding (CMC higher than C) and 4 h (Pe, G and CMC higher than C).

5. Compared with diet C, the rate of gastric emptying of digesta was significantly slower for diet G, 1, 2 and 4 h after feeding, and 2 and 4 h after feeding for diet CMC.

6. The rates of gastric emptying of digesta components were not significantly reduced by dietary fibre except for dry matter (DM) (diet CMC 2 h and diet B 4 h after feeding), total nitrogen (TN)(diet G 2 h after feeding) and total glucose (diet Pe 2 h after feeding).

7. There were no significant effects of diet on trichloroacetic-acid-soluble N:TN.

8. When gastric emptying was expressed in terms of half-time (T59) values, significant increases (compared with diet C) were found for digesta (diets G and CMC), DM (diet WB) and TN (diet G).

9. The apparent viscosity of the gastric digesta was significantly higher when diets Pe, G, and CMC were given than diets C or WB. Diets Pe and CMC were very viscous in the meal before ingestion, but diet G was not; its high viscosity developed after it had reached the stomach.

10. It is concluded that although those types of dietary fibre which increased meal or gastric viscosity reduced the rate of gastric emptying of digesta, this effect was confined to the liquid phase, because DM, total glucose and TN emptying were largely unaffected. The hypothesis that a reduced rate of gastric emptying may be an important determinant of the decreased rates of glucose absorption observed when such sources of dietary fibre are eaten is not supported by the results presented.