1. Net amino acid uptake, and incorporation into protein have been measured in vitro in the presence and absence of porcine growth hormone (GH) in muscle from intact rabbits fed for 5 d on low-protein (LP), protein-free (PF) or control diets.

2. In muscle from control and LP animals GH had no effect on the net amino acid uptake but stimulated amino acid incorporation into protein, although this response was less in LP animals than in control animals.

3. In muscle from PF animals, GH stimulated both amino acid incorporation into protein and the net amino acid uptake, a type of response which also occurs in hypophysectomized animals. The magnitude of the effect of GH on the incorporation of amino acids into protein was reduced in muscle from PF animals.

4. The effect of GH on the net amino acid uptake in PF animals was completely blocked by cycloheximide; the uptake effect of GH in these animals was dependent therefore on de novo protein synthesis.

5. It is proposed that in the adult the role of growth hormone in protein metabolism is to sustain cellular protein synthesis when there is a decrease in the level of substrate amino acids, similar to that which occurs during a short-term fast or when the dietary protein intake is inadequate.

1. [35S]sulphate was used to measure the apparent turnover of sulphate, sulphide and microbial-protein-S in the rumen contents of four sheep that were intraruminally infused with 10 g sodium sulphate/d alone, or together with 126 mg sodium molybdate (50 mg molybdenum/d).

2. Infusion of molybdate increased the concentration of sulphate in rumen fluid from 2.2 to 7.2 μg S/ml and decreased the rate of reduction of sulphate to sulphide by 50%. Although the rate of sulphide production was slower, the concentration of sulphide in rumen contents was increased. A dual role for molybdate in the metabolism of sulphide in the rumen is suggested to explain these changes.

3. In animals that were not infused with molybdate, only one-third of the S (3.0 g/d) that passed through the sulphate pool in rumen fluid was converted to sulphide, decreasing to one-sixth when molybdate was infused.

4. The turnover of S amino acids in microbial protein was not significantly affected by molybdate. Only 52–57% of the S amino acid content of microbial protein was synthesized de novo by way of the sulphide pool.

1. Monosodium glutamate (MSG) was administered by various methods to mice and rats of various ages and the incidence of obesity was later measured.

2. Newborn mice were injected subcutaneously with 3 mg MSG/g body-weight at 1, 2, 3, 6, 7 and 8 d of age; 16% died before weaning. Of the survivors, 90% or more became markedly obese. Mean carcass lipid content was increased by about 120% in both sexes at 20–30 weeks of age. In male mice, MSG treatment increased body-weight and epididymal fat pad weight, and greatly decreased adrenaline-stimulated lipolysis in isolated fat cells. Body-weight of females was not increased significantly. Food intake was not increased in either sex from weeks 13 to 15. Blood glucose level was not generally increased by MSG but some of the male mice had abnormally high values.

3. Obesity was not detected in the offspring of female mice that had received 100 g MSG/kg diet, either from 3 weeks before mating until weaning, or from the 14th day of pregnancy until weaning.

4. Intraperitoneal injection of 10 mg MSG/g body-weight (in two doses) at weaning increased carcass lipid content in female mice by 34% by 23 weeks of age, but female rats were not affected.

5. The addition of 20 g MSG/l to the drinking-water from weaning onwards did not increase carcass lipid content in female rats or mice.

6. The addition of 20 g MSG/kg diet from weaning onwards did not alter body-weight or carcass lipid content in male and female rats by 14 weeks of age.

7. The obesity induced in mice by MSG was not associated with hyperphagia, unlike genetic obesity and obesity induced by gold thioglucose (GTG).

8. All types of mouse studied, obese and lean, had essentially the same linear relationship between carcass water content and carcass lipid content.

9. Although MSG-obese mice could not readily be differentiated from normal mice by the increase in body-weight, which was only about 10% compared to 50–120% for genetic and GTG-induced obesity, the proposed schedule of injections in the newborn was almost 100% reliable in inducing a high extent of adiposity.

1. Sixty-four male rats were fed on a nutritionally complete diet containing 30% of the dietary energy as fat. For thirty-two rats (control) the fat source was maize oil; for the remaining thirty-two rats (experimental) the fat source was triundecanoin–maize oil (7:3, w/w).

2. After 6 weeks, groups of control and experimental rats were fasted and killed on days 0, 1, 2 and 4 of the fasting period. In the experimental group, adipose-tissue fatty acids contained, on average, 246 mmol undecanoic acid/mol total fatty acids. In contrast, the adipose tissue of the control group did not contain odd-carbon-number fatty acids.

3. Plasma glucose levels were significantly higher for all fasted experimental groups and blood ketone levels were significantly lower for these groups.

4. Thus, during prolonged starvation, animals which accumulated odd-C-number fatty acids resisted the development of ketosis. It appeared that odd-C-number fatty acids mobilized from fat depots during fasting may provide their terminal three-C residues for gluconeogenesis rather than for acetyl-CoA production, thereby allowing for better maintenance of blood glucose and insulin levels than in control animals.

5. It is concluded that the lower acetyl-CoA production and higher blood insulin levels reduce ketogenesis.

1. In the first experiment sheep taken from pasture were given a low-protein diet for 6 weeks in individual pens. Then, for 1 week, groups were given a supplement of lucerne chaff, safflower meal or lucerne chaff plus safflower meal. In the second experiment eighteen sheep maintained on lucerne chaff rather than pasture were then depleted of protein to a greater extent by feeding on a restricted low-protein diet. Six of the sheep received a supplement of molasses throughout the period of protein depletion while six of the sheep on the basal ration received a supplement of safflower meal after 6 weeks on the low-protein diet.

2. The urea tolerance of the sheep, as indicated by blood ammonia levels after oral dosing with aqueous solutions of urea, was determined after the period of supplementation. ‘Arginine synthetase’ activity (combined activities of argininosuccinate synthetase (EC 6.3.4.5) and argininosuccinate lyase (EC 4.3.2.1)) was determined in liver samples obtained by biopsy at various intervals during the experiment.

3. Supplementation for 7 d with 73 g crude protein (nitrogen × 6.25)/d increased the tolerance to urea, as indicated by reduced blood NH3 levels, and also increased ‘arginine synthetase’ activity.

4. Giving supplements of molasses delayed the onset of urea toxicity but not the extent of toxicity.

5. It is suggested that short-term feeding of protein concentrates to sheep before giving urea supplements can increase their tolerance to urea.

1. When nineteen ‘free-living’ male students, who normally ate 231 (SEM 14) g white bread/d changed to wholemeal bread for a 19-week period, there was no significant change in body-weight, plasma cholesterol or plasma triglyceride levels. These values, as well as plasma concentrations of calcium, phosphate, urate and haemoglobin, remained essentially the same as those for a control group.

2. Increasing the wheat-fibre intake by eating wholemeal bread is not an effective method for reducing blood lipid levels, at least in healthy young men with a moderate bread intake.

1. The effect of increasing dietary protein content on the amount of faecal nitrogen was measured in six normal subjects and five subjects without functioning colons (three with ileostomy and two with ileo-rectal anastomosis).

2. There was a significant increase in the amount of faecal N with increased dietary protein content in the subjects without functioning colons.

3. In normal subjects with intact colons, faecal N content was found to be lower than that in subjects without colons, and furthermore there was no significant variation with diet.

4. The source of the increase in faecal N with increased dietary protein content in subjects without functioning colons is discussed and the significance of these findings in relation to the efficiency of protein absorption is considered.

1. A control diet and diets containing 150 g non-irradiated or 150 g irradiated mangopulp/kg were given to female rats from day 15 of the gestation period until weaning in trials 1 and 2, and from 40 d before mating until 28 d post weaning in trial 3.

2. Food intake and dry-matter digestibility were similar with all diets.

3. There were no significant differences between animals given the different dietary regimens in the daily body-weight changes of weanling males, pups, nursing females or females during the immediate postlactation period.

4. No differences in haematological or blood chemistry values were found which could be attributed to the ingestion of irradiated mangoes. There was no evidence for the presence of any toxic substances in the irradiated-mango-pulp diet.

5. Gross pathological observations revealed no aberrations which could be related to the ingestion of irradiated mangoes.

6. It may be concluded that the wholesomeness of mangoes was not affected by gammairradiation at a dose of 75 krd.

1. The solubility of fatty acids in aqueous media containing bile salts alone and in admixture with either lecithin (phosphatidylcholine) or phosphatidylethanolamine was determined.

2. Over the pH range 2.0–7.4, the order of fatty acid solubility in aqueous solutions containing bile salts was linoleic > oleic > elaidic > palmitic > stearic. The solubility of each fatty acid increased as the pH of the micellar solution increased.

3. Addition of lecithin to aqueous solutions of bile salts greatly increased the solubility of palmitic acid and stearic acid.

4. In the presence of bile salts and lecithin, the solubility of oleic acid and elaidic acid decreased with increasing pH of the micellar solution, indicating a competitive effect between the fatty acid anions and lecithin. The solubility of linoleic acid increased linearly with lecithin concentration.

5. Phosphatidylethanolamine as an additive to bile salts increased the solubility of both saturated and unsaturated fatty acids in the pH range 2.0–7.4. The effectiveness of phosphatidylethanolamine as an amphiphile was similar to that of lecithin, although at pH 3.0 fatty acid solubility was greater in the presence of phosphatidylethanolamine.

6. The significance of these findings is discussed in relation to the intestinal absorption of fatty acids in sheep.

1. The solubility of fatty acids in aqueous solutions containing bile salts and lysolecithin at pH values between 2.0 and 7.4 was studied. Both the 1-acyl and 2-acyl isomers of lysolecithin increased the solubility of fatty acids to the same extent, the order of solubility being linoleic > oleic > elaidic > palmitic > stearic.

2. The influence of the products of phospholipolysis of lecithin on palmitic acid solubility was determined. On a molar basis, lysolecithin was more effective than were bile salts in promoting the solubilization of the fatty acid.

3. In bile salt solutions in which the phospholipid concentration was constant on a molar basis, the solubility of palmitic acid decreased linearly with the progressive replacement of lecithin by lysolecithin. Palmitic acid was solubilized to the same extent on replacing lecithin with lysolecithin on a constant weight basis.

4. In bile salt solution containing lysolecithin and oleic acid in equimolar amounts, the solubility of palmitic acid was similar to that in bile salt solutions containing lecithin in equivalent proportion.

5. The results are discussed in relation to the action of phospholipolytic activity on the intestinal absorption of fatty acids in sheep.

1. The effect of consuming the same total amount of food in either one large meal or several small meals per d was studied using weanling male rats.

2. The increase in total body-weight was the same in both instances, but the weights of the liver, kidneys, femur, small intestine and stomach were greater, and those of the spleen and residual carcass were smaller, in meal-eating rats than in continuously fed control animals. These differences persisted into the adult state.

3. No differences in gross chemical composition were found between the corresponding organs of the two groups of rats, and the differences in weight appeared to be the result of changes in the general growth rate of individual organs.

4. The hypertrophy of the kidneys in meal-eaters was due to an increase in mean cell size, but the increased weight of the liver and reduced weight of the spleen appeared to be largely the result of changes in the number of cells present.

1. Ninety-one families containing 140 children under 4 years of age at enrolment were studied. At 1-monthly intervals, the children were weighed and measured and qualitative information about feeding habits was obtained. Weighed dietary surveys for periods of 5 d were made at approximately 8 months, 20 months, 3 years and 5 years of age; there were forty-six failures in 260 surveys attempted.

2. At the four specified ages, mean energy intakes were 3.75, 5.03, 5.82 and 6.75 MJ (896, 1203, 1392 and 1613 kcal)/d respectively. At 8 months, milk products provided on average, 43% of the total energy intake and commercial baby foods provided 17%. These values decreased to 21 and 2% respectively at 20 months and there was little further change thereafter.

3. Average intakes of energy and of most nutrients met recommended intakes (Department of Health and Social Security, 1969). Iron intakes were marginal, and vitamin D intakes were low.

4. The energy intake of boys was significantly higher than that of girls at 3 years of age, but the boys were not significantly heavier. The energy intake of children from ‘manualworker’ families was higher than that from ‘non-manual’ families. Similarly, the energy intake of children from larger families was higher than that of children from smaller families.

5. Energy intakes were correlated with body-weights and with rates of gain in weight. Irrespective of body-weight, ‘big eaters’ at 20 months tended to be ‘big eaters’ at 3 years also.

1. The occurrence of biotin deficiency and fatty liver and kidney syndrome (FLKS) in chicks was studied using a 2 × 2 × 2 × 2 factorial-design experiment in which the variables were dietary biotin, fat and protein, and starvation.

2. The severity of biotin deficiency, using growth retardation and severity of dermal lesions as criteria, was least when the low-biotin diet also contained low levels of fat and protein. Addition of fat or protein increased the severity of the deficiency. Tissue fatty acid composition was affected by biotin deficiency only in those birds given the low-protein, low-fat diet. The main change was an increase in the ratio, 16:1 fatty acids:18:0 fatty acids. Plasma glucose and free fatty acid levels in non-fasted birds were unaffected by the dietary variables.

3. Mortality from FLKS with the diet containing low biotin, fat and protein levels was 52% at 28 d, but was reduced or eliminated when the dietary level of any of these ingredients was increased.

4. Starvation considerably increased the incidence of FLKS in the period immediately after fasting, and also affected plasma glucose and free fatty acid concentrations. Liver fatty acid composition indicated an increase in the proportion of 18:0 at the expense of 16:1 and 18:1, irrespective of diet, except when the bird developed FLKS, when 16:1 and 18:1 concentrations increased in proportion, at the expense of 18:0.

5. The relationship between biotin deficiency and FLKS, and a possible mechanism for the induction of FLKS by starvation are discussed.

1. A study of ammonia and urea metabolism in sheep was made using isotope dilution techniques with (15NH4)2SO4, [15N]urea and [14C]urea in order to determine quantitatively the movements of urea-N and NH3-N throughout the body of normal, feeding sheep.

2. Single injections of 15N-labelled compounds were made into the rumen fluid NH3, caecal fluid NH3 and the blood urea pools, in order to estimate the rates of flux through, and the transfer of N between, these and other nitrogenous pools in the body. 51Cr EDTA was injected into the rumen and caecum with (15NH4)2SO4 to allow estimation of fluid volumes and to provide an indication of mixing, and of times of transit of isotopes between different sampling sites in the digestive tract.

3. The sheep ate approximately 22 g lucerne chaff/h and the mean dietary N intake was 16.3 g/d.

4. The rate of flux of NH3 through the rumen NH3 pool was 15.0 g/d (i.e. 90% of the dietary N ingested; however, this amount also included N from plasma urea (1.1 g/d) and other endogenous sources including NH3 derived from caecal NH3 (0.4 g/d).

5. Only 40% of the N in isolated rumen bacteria was derived from NH3, indicating that a considerable proportion of their N requirements were obtained from compounds other than NH3 (e.g. peptides and amino acids).

6. There was evidence of recycling of N between nitrogenous pools in the rumen, probably through rumen NH3 → microbial N → NH3.

7. It was estimated that 5.3 g blood urea-N/d entered the digestive tract: 20% of this urea was degraded in the rumen, 25% in the caecum and the remainder was apparently degraded elsewhere; there was evidence of urea degradation in the large intestine posterior to the caecum and it is suggested that urea degradation and absorption of the resultant NH3 may occur in the ileum.

8. Of the 4.8 g N/d entering the caecal NH3 pool, 4.2 g N/d left and did not return and the difference (0.6 g N/d) was recycled, possibly through caecal NH3 → microbial N → NH3.

9. A large proportion of the NH3 entering the caecal NH3 pool (70% or 3.2 g N/d) was apparently derived from degradation of nitrogenous products, other than urea, including rumen microbial N (1.0 g N/d) passing undigested from the small intestine.

10. Less than half the NH3-N of caecal origin entering the rumen passed through the blood urea pool; the remainder was apparently transported as other nitrogenous compounds in the blood or body fluids.

11. The results of the three experiments were combined in a general three-pool, opencompartment model which formally recognizes an unlimited number of other unspecified, interconnected pools together comprising the whole-animal system. Rates of flux through, and transfer of N between these and other nitrogenous pools in the body were calculated by solving this model and the information derived has been applied to whole-animal models with a view to subsequently using these models in computer simulation studies.

1. The results of isotope tracer studies of the dynamics of nitrogen metabolism in mature sheep were used to construct a seven-pool mathematical model.

2. The model was extended to a nine-pool model, which incorporates lags describing the time taken for the passage of digesta through the gut of sheep.

3. Simulation studies using these models satisfactorily predicted results of independent experiments.

4. The dynamics of N metabolism in sheep appear to be best approximated by first-order kinetics; that is, many of the important N transport processes are substantially linear or concentration-dependent.

1. Escherichia coli was grown on 14C-labelled glucose and fractions representing ‘whole cells’, ‘cell contents’ and ‘cell walls’ were administered orally to rats.

2. 14C appearing as 14CO2 in the expired air and as unidentified radioactive products in urine and faeces was measured until the cumulative recovery showed little change with time.

3. All fractions were digested. The digestibility of cell waslls was less than that of the other fractions.

4. There was considerable variation among individual rats.