1. Eight pigs with a mean weight of 48 kg were given, at a constant daily rate, diets of low (0.15) or high (0.30) protein content, very deficient in lysine, with or without a supplement of L-lysine (3.7 g/kg).

2. Measurements of nitrogen and energy metabolism were made in four successive 14 d periods in a Latin-square design.

3. The rate of protein accretion was substantially increased by increases in both protein and lysine supply, but the rate of heat production was not significantly changed.

4. The rate of fat deposition varied inversely with the rate of protein accretion, being reduced by both protein and lysine supplements.

5. The relation between heat production and protein accretion (allowing for a constant energy cost of fat deposition) suggested that heat production increased with additional protein accretion less when protein quality was improved than when more protein was given.

1. Six steers implanted with 300 mg trenbolone acetate and six steers not implanted were fed on low protein, low-quality-roughage diets ad lib. in two experiments. The steers were Hereford (Bos taurus) × Brahman (Bos indicus) crossbreds (50:50), initially of about 400 kg mean live weight (LW). In the first experiment of 8 weeks duration roughage was given alone. In the second experiment of 6 weeks duration the diet was supplemented with 100 g urea and 4.6 g sulphur daily. The same steers were implanted in each experiment. At the conclusion of each experiment metabolic rate was measured after a 72 h fast.

2. In the first experiment control and implanted steers had similar rates of LW loss (0.57 and 0.59 kg/d respectively). Implanted steers had significantly (P < 0.01) lower feed intakes (12.8 v. 10.9 g dry matter (DM)/kg LW), significantly (P < 0.01) lower fasting metabolic rates even after adjustment for intake (83.3 v. 74.5 kJ/kg per d) and significantly (P < 0.01) lower plasma insulin concentrations (24 v. 19 μunits/ml). Differences in plasma concentrations of free 3,5,3′-triiodothyronine (T3), non-esterified fatty acids and urea-nitrogen were not significant.

3. In the second experiment intake of the supplement diet was similar in both control and trenbolene acetate treated steers (19.5 and 20.0 g DM/kg LW respectively). LW gains were 0.23 and 0.41 kg/d for control and implanted steers respectively, the difference being s ignificant (P < 0.05). Fasting metabolic rate (76.9 v. 70.7 kJ/kg per d) was significantly (P < 0.05) lower in implanted steers.

1. For a period of 24 d rats were given diets containing either casein or pea (Pisum sativum) protein at two different concentrations (180 and 120 g/kg) without or with cysteine or cysteine + methionine supplementation.

2. The effects of these diets on levels of blood and liver reduced glutathione (GSH) and serum thyroid hormones were studied.

3. When compared with the 180 g casein/kg diet, the 120 g casein/kg diet decreased liver GSH and serum thyroid hormone concentrations. These changes were related to dietary cysteine supply since supplementation induced an increase in these variables.

4. When compared with 180 g pea protein/kg diet, the 120 g pea protein/kg diet decreased liver GSH and serum thyroid hormone concentrations. These changes could not be corrected by cysteine or cysteine + methionine supplementation.

1. Long-term exposure of the fruit bat Rousettus aegyptiacus to nitrous oxide, which inactivates methylco balamin, leads to neurological impairment and ataxia.

2. In N2, O-exposed animals, liver concentrations of total folates and methyl folates decreased to less than one fifth that of control animals. Pediococcus cerevisiue-active folates were also reduced.

3. In brain, there were no changes in total or methyl folates, but P.cerevisiae-active folates were lower in N2, O-exposed animals.

4. Supplementation with methionine retarded the development of neurological impairment and the fall in liver total and methyl folates, but not that in P. cerevisiae-active folates.

5. Supplementation with serine failed to retard the development of neurological impairment or fall in hepatic folates.

6. The present results suggest that the N2O-induced neurological impairment in the bat is not related to depletion of cerebral folates, but do not exclude changes in the subcellular distribution of folates.

1. The interrelations between protein accretion and whole-body protein turnover were studied by varying the quantity and quality of protein given to growing pigs.

2. Diets with 150 or 290g lysine-deficient protein/kg were given in hourly meals, with or without lysine supplementation, to female pigs (mean weight 47 kg).

3. After the animals were adapted to the diets, a constant infusion of [14C]urea was given intra-arterially for 30 h, during the last 6 h of which an infusion of [4,5-3H] leucine was also infused at a constant rate. At the same time, yeast-protein labelled with 15N was given in the diet for 50 h.

4. The rate of urea synthesis was estimated from the specific radioactivity (SR) of plasma urea. The rate of leucine flux was estimated from the SR of plasma leucine. The irrevocable breakdown of leucine was estimated from the 3H-labelling of body water. Total N flux was estimated from the 16N-labelling of urinary urea.

5. Addition of lysine to the low-protein diet significantly increased N retention, with a substantial reduction in leucine breakdown, but there was no significant change in the flux of leucine or of total N.

6. Increasing the quantity of the unsupplemented protein also increased N retention significantly, with concomitant increases in leucine breakdown and in the fluxes of leucine and of total N.

7. It is concluded that a doubling of protein accretion brought about by the improvement of dietary protein quality is not necessarily associated with an increased rate of whole-body protein turnover.

1. Kinetics of physiological doses of D-α-[5-Me-3H]tocopherol(200 μCi) administered to twenty-four sheep were studied using one of four routes: intravenous, oral (capsules), intraruminal and intramuscular.

2. Blood samples were withdrawn from the jugular vein periodically for 96 h after the intravenous and oral administrations, for 168 h after the intraruminal administration and for 216 h after the intramuscular administration.

3. The study indicated that the biological availability of α-tocopherol followed the order intravenous > intramuscular > oral > intraruminal.

4. The rate of elimination was in the order intravenous > oral > intraruminal ˜ intramuscular.

5. The intravenous route was fitted with a three-compartment model, whereas the other routes exhibited a good fit for either a one- or two-compartment model.

1.The effect of sugar fatty acid esters (SFEs; currently used as food additives for human consumption) on rumen volatile fatty acids (VFA) and gas production was studied with sheep rumen contents in vitro.

2. Some SFEs having monoester contents of more than 70 % increased the molar proportion of propionate in conjunction with reduction in the acetate: propionate ratio when the individual SFE was added to rumen contents in a final concentration of 4 g/l. Laurate sugar ester was the most potent propionate enhancer and rumen gas depressor, the effective dose being as low as 1 g/l in a final concentration. Fatty acid esters other than SFEs had little, if any, effect on rumen VFA production and their molar proportions.

3. Approximately 50% of laurate sugar ester was hydrolysed by in vitro incubation with rumen fluid for 2 h. The addition of fatty acids and sucrose was also effective in the alterations of rumen VFA and gas production. However, the effect of SFEs on in vitro rumen fermentation was significantly greater than that of their constituent fatty acids or sucrose, or both. Accordingly, the effect appeared to be ascribed to the complex action of SFE itself and to its constituents, free fatty acids and sucrose.

4. SFEs, at the level of 4 g/l, reduced substantially the froth formation (ingesta volume increase) and seemed to be effective for the prevention of bloat.

1. Studies have been made of the time-sequence of protein metabolic and hormonal changes following an abrupt increase in carbohydrate or fat intake. [3H]leucine and [14C]urea were infused for 72 h, via the aorta, into fourteen female pigs (30–38 kg body-weight). At 24 h after the start of the infusion their feed was either changed to one of two isonitrogenous diets containing additional starch (group BS, five animals) or fat (group BF, five animals), or remained unaltered (group BB, four animals). The distribution space of urea was measured by the dilution of a single dose of [14C]urea given both 48 h before and 48 h after the change in diet. The changes in the concentration and specific radioactivity of blood leucine were used to infer changes in protein turnover and those of plasma urea to measure total amino acid catabolism. The concentrations of blood glucose and plasma insulin and cortisol were also measured at approximately two-hourly intervals for the 48 h period following the change in diet.

2. Within 4 h of either change in diet blood leucine concentration was lowered and the leucine specific radioactivity was raised above that in group BB, but after 24 h both the concentration and specific radioactivity of leucine returned to values similar to those in group BB. Eventually the blood leucine specific radioactivity was slightly but not significantly reduced below that of group BB.

3. The addition of starch to the diet significantly reduced the synthesis and concentration of urea within 4 h but, although the addition of fat to the diet eventually lowered the urea concentration and synthesis, both changes were delayed for 18–24 h.

4. In group BS plasma glucose and insulin rose after the addition of starch, but after 24–36 h both returned to values that were the same as those in the animals that received the same diet throughout (group BB). The addition of fat to the diet altered neither blood glucose nor plasma insulin concentrations. The addition of either carbohydrate or fat to the diet eventually reduced pIasma cortisol concentrations, but the change did not occur until 24 h after the change in diet.

5. The results suggest that alterations in non-protein energy supply exert their immediate effect on the degradation of whole-body protein. They do not exclude the possibility that these early changes may reflect opposing changes at different sites. The results also suggest that the rate of urea synthesis may be controlled by the balance between the concentrations of insulin and cortisol, but that under the conditions of these experiments there was little relation between these hormones and the turnover of body protein as measured by the turnover of blood leucine.

1.A significant linear increase in egg-shell defects from 60-week-old laying hens, and corresponding significant linear decreases in various egg-shell-quality measurements, were observed in response to increasing concentrations of sodium chloride in the drinking water, to the maximum concentration of 600 mg/l used in the present study.

2. The incidence of damaged egg shells was increased 3-fold by including NaCl in the drinking water at a concentration of 600 mg/l.

3. Shell defects declined when birds were placed on normal water for 5 weeks but were still 1.4- to 2.1-fold greater than control values.

4. After an induced rest from lay on normal water, shell defects were still 1.3- to 3.2-fold greater in birds which had previously received the NaCl in the drinking water.

5. The increased incidence of shell damage was not related to decreased food intake or increased egg weight or production.

1. The cellular proteins of Butyrivibrio jibrisolvens, Lactobacillus casei, Megasphaera elsdenii, Selenomonas ruminantium and Streptococcus bovis were labelled by growth in the presence of L-[14C]leucine, and the breakdown of labelled protein was measured in incubations of these bacteria with rumen fluid to which unlabelled 5 mM-L-leucine was added. The rate of protein breakdown was estimated from the rate of release of radioactivity into acid-soluble material.

2. Protein breakdown occurred at different rates in different species. The mean rates for B. fibrisolvens, L. casei, M. elsdenii, Sel. ruminantium and Str. bovis were 28.6, 18.1, 17.7, 10.5 and 5.3% /h respectively in samples of strained rumen fluid (SRF) with different protozoal populations. Rates of 3% /h or less were found in SRF from ciliate-free sheep or in faunated SRF from which protozoa had been removed by centrifugation. Further removal of mixed rumen bacteria had little effect. Suspensions of washed protozoa degraded bacterial protein at rates which were of the same order as those found in SRF.

3. The rate of breakdown of bacterial protein in different samples of SRF tended to increase as the numbers of small entodiniomorphid protozoa increased. The numbers of larger entodiniomorphs and holotrichs had no obvious influence on this rate.

4. Autoclaved and u.v.-treated bacteria were generally no different from live bacteria in their susceptibility to breakdown in SRF from faunated sheep, indicating that endogenous protein turnover was not a significant cause of bacterial protein catabolism.

5. The rate of bacterial protein breakdown was unrelated to the proteolytic activity of SRF.

6. It was concluded that predation by small protozoa is by far the most important cause of bacterial protein turnover in the rumen, with autolysis, other lytic factors and endogenous proteolysis being of minor importance.

1. At 16 h after the rapid injection of 99Mo-labelled compounds into the rumen of sheep maintained on dried grass (6.2 mg molybdenum/kg dry matter (DM), 4.3 g sulphur/kg DM), labelled thiomolybdates associated with the digesta solids or bound to plasma macromolecular species were displaced from their carriers in vitro and identified by Sephadex G25 chromatography.

2. After molybdate injection, the thiomolybdates displaced from rumen, duodenal and ileal solids were predominantly the trithio- and tetrathio- species. Dithiomolybdate was present to a relatively minor extent. Trace amounts of di- and trithiomolybdates were detected in the liquid phase of digesta from the duodenum.

3. Whether injected into the rumen as molybdate or tetrathiomolybdate, bound 99Mo appearing in plasma was present mainly as di- and trithio- species. The tetrathio- species appeared in trace amounts in plasma only after tetrathiomolybdate injection, despite its existence almost exclusively in this form in rumen digesta.

4. The present study provides direct evidence for thiomolybdate synthesis within the rumen and indicates that while the effects of thiomolybdates in inhibiting copper absorption are likely to be due to tri- and tetrathio- molybdates, post-absorptive effects on Cu metabolism are probably due to di- or trithiomolybdate.

1. Cockerels (1-d-old) received over a period of 4 weeks, a balanced diet containing either safflower oil (diet S) or linseed oil (diet L) as a source of polyunsaturated fatty acids (PUFA). Body-weight, and weights of cerebrum and cerebellum increased at similar rates in the two dietary groups. The total fatty acids (FA) of the cerebellum differed from the cerebral FA by their higher PUFA and oleic acid contents and their lower stearic acid level. During the 3rd week of life there was a spurt in accretion of PUFA in the cerebellum, but not in the cerebrum. At the end of the experimental period phosphatidylethanolamine was present at twice the concentration in the cerebellum, compared with the cerebrum.

2. Diets S and L resulted in extensive mutual replacement of ω6- and ω3-FA in brain, without any significant change in the total PUFA. Brain oleic acid concentration was higher in the diet-L group than in the diet-S group, but saturated FA were not affected by the dietary treatments.

3. These results may be relevant to basic brain biology and to chick nutritional encephalomalacia (NE). This disease, which specifically affects the cerebellum and is readily induced by diets supplying linoleic acid but deficient in vitamin E, usually reaches its highest incidence during the 3rd week of life and may thus be related to the cerebellar PUFA spurt that occurs at that time. The fact that NE was induced by linoleic acid, while α-linolenic acid exerted a protective action, points to an overproduction of arachidonic-derived eicosanoids as a factor in the etiology of the cerebellar lesion and possibly a structural change due to a loss of docosahexaenoic acid and gain of arachidonic acid in the chicks given diet S.

1. An experiment was conducted using three non-lactating cows completely maintained by infusions of volatile fatty acids into the rumen, and casein into the abomasum. Plasma insulin responses to propionic acid, glucose or casein were recorded. Further information was obtained using protein-free infusions.

2. When part of the propionic acid was infused into the rumen in a twice-daily 3 h dose and the remainder infused continuously with acetic and butyric acids and casein, there were large increases in the concentrations of propionic acid and insulin in the jugular blood. When glucose, corresponding in energy to that supplied by the intermittent propionic acid infusions was similarly infused, the plasma levels of glucose and insulin were increased. Glucose appeared to stimulate a greater increase in insulin than did propionic acid. Casein infused into the abomasum in intermittent doses produced a rise in plasma insulin, but smaller than that observed with propionic acid or with glucose.

3. The protein-free infusion was characterized by a lower concentration of insulin in the blood plasma, a reduction in plasma urea and free amino nitrogen and unchanged plasma glucose.

1. Adolescent cockerels of a laying strain were prepared with catheters whose tip lay in the hepatic portal vein, to study the effect of 3-h infusions of nutrients on food intake.

2. Lysine, infused into the hepatic portal vein at rates of 150–450 mg/3 h reduced 3-h food intake by up to 58%, for a period of 6 h in previously starved birds, but had no effect on birds allowed free access to food. Infusions made into the jugular vein had no effect, suggesting a role for the liver in monitoring lysine levels.

3. Portal infusion of leucine had a delayed effect while ammonium chloride, infused at isomolar rates to those of the lysine infusions, had very little effect on intake.

4. The results support the concept of liver sensitivity to amino acids, but the mode of action is not clear; it appears not to be via the effects of ammonia.

1. The histidine requirement of growing kittens was determined from an experiment in which forty-eight kittens were randomly allocated to six amino acid-based diets supplying: 1.0, 1.5, 2.0, 2.5, 3.0 or 4.5 g histidine base/kg diet.

2. By 48 d it was obvious that 1.0 and 1.5 g histidine/kg diet were grossly inadequate so the kittens receiving these two diets were removed from the experiment. The other four groups of kittens continued to receive their diets for a total of 128 d.

3. Mean daily weight gain, nitrogen retention and food intake attained plateau values at 2.1 g histidine/kg diet.

4. Blood samples taken at 25 and 48 d after kittens were given the diets showed a significant effect of dietary histidine on haemoglobin (Hb) concentration. Hb and packed cell volume (PCV) attained asymptotic values at 3.0 g histidine/kg diet at 48 d. At 128 d, kittens consuming diets containing 2.0–4.5 g histidine/kg had similar Hb and PCV values.

5. Cataracts of both eyes were observed in two of nine female kittens which had received diets containing either 2.0 or 2.5 g histidine/kg.

6. A concentration of 3 g histidine/kg diet is recommended as a practical guide for feeding kittens.

7. There was a rectilinear relation (r2 0.99) between the logarithm of the histidine concentration of plasma and the concentrationof histidine in the diet over the range 1.5–3.0 g histidine/kg diet.

1. Digestive efficiencies of fibre components and retention time of digesta in the whole gut and in the large intestine were measured in rabbits, guinea-pigs, hamsters and rats when given a lucerne (Medicago saliva)-containing diet.

2. Co-EDTA and chromium-mordanted cell-wall constituents of Italian ryegrass (Lolium multiflorum L.) were used as liquid- and solid-phase markers respectively. Both markers were mixed with the experimental diet and given after digestion trials.

3. Mean retention times of each marker were calculated from time-course changes in concentrations of the markers in faeces. The mean retention times of the markers in the large intestine were calculated from exponential slopes fitted to the time-course changes of faecal concentrations of the markers.

4. The digestibilities of crude fibre, neutral-detergent fibre and acid-detergent fibre were highest in the guineapigs, followed by the hamsters, and lowest in the rabbits and rats.

5. The mean retention times of Cr in the whole tract were longer in the larger animals and shortest in the hamsters. The mean retention times of Cr in the large intestine were longest in the guinea-pig followed by the hamsters and the rats. The rabbits had an extremely short retention time of Cr in the large intestine.

6. These results suggest that the retention time of solid digesta in the large intestine can explain the difference in the digestive efficiencies of fibre components amongst non-ruminant small herbivores whereas retention of digesta in the whole gut is not related to the digestibility of fibre components.

1. In Expt 1, fractional synthesis rates (FSR) of tissue protein were measured along the gastrointestinal tract (GIT) of six 1-week-old, milk-fed lambs by using a large amount of L-[3,4(n)-3H]valine.

2. In Expt 2, eighteen lambs were used to determine the fractional growth rate (FGR) of gastrointestinal tissue protein.

3. FSRMinimum(Min) and FSRMaximum(Max) were calculated assuming plasma or tissue homogenate free valine specific radioactivity was representative of the valine precursor pool for protein synthesis. There were no significant differences between FSR(Min) and FSR(Max) in any gastrointestinal tissue of lambs used in Expt 1 (P > 0.05). FSR gradually and significantly (P > 0.05) increased from the oesophagus (FSR(Max)26.5%/d). reticulo-rumen (30.1%/d), omasum (41.0%/d) and abomasum (56.1%/d) to small intestine (87.5%/d), and then declined significantly (P < 0.05) towards the caecum (45.2%/d) and the colon (38.4%/d). No significant differences were observed between FSR in the duodenum, jejunum or ileum (P > 0.05).

4. FGR ranged from 2,6%/d in the oesophagus to 8,7%/d in the omasum. The ratio, FGR:FSR, which reflected the efficiency of protein deposition, was at a maximum in the stomachs and caecum and at a minimum in the small intestine.

5. The relative contribution of the oesophagus, stomachs, small intestine and large intestine to GIT protein synthesis was 1, 13, 76 and 10% respectively. The GIT accounted for approximately 11.5% of whole-body protein synthesis.

1. The activities of two hepatic enzymes that participate in the regulation of amino acid oxidation and urea synthesis were measured in lactating rats (day 15 of lactation) and virgin controls. The enzymes were alanine aminotransferase (EC 2. 6. 1.2) and argininosuccinate synthase (EC 6. 3. 4.5). Carcasses of the dams were also analysed.

2. Changes in the activities of both enzymes in dams fed ad lib. on a diet containing an excess of protein indicated that amino acid oxidation was depressed. In dams restricted in protein to the level of intake of their controls but allowed to satisfy their needs for energy, enzyme activities were significantly reduced. In these animals lean tissue catabolism supplemented the dietary protein supply.

3. This adjustment in protein metabolism which effectively spares protein for milk-protein synthesis could be explained either by a reduction in the availability of substrate in the liver, or by the intervention of an anabolic hormone secreted in lactation.