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.