1. The effects of feeding either high-protein (HP) or low-protein (LP) diets between 1.8 and 15 kg live weight (LW) and a low-energy (LE) or high-energy (HE) intake subsequently on the cellularity of muscle and adipose tissue in pigs growing to 75 kg LW were investigated.

2. The effects of the nutritional treatments on muscle tissue were assessed from the weight and DNA content of the m. adductor. For adipose tissue the total DNA content and fat cell size of the subcutaneous adipose tissue contained in the left shoulder joint were determined.

3. Feeding the LP diets in early life reduced the weight and DNA content of the m. adductor (P < 0.01) and increased fat cell size (P < 0.01) at 15 kg LW.

4. Subsequent to 15 kg there was an almost linear increase in muscle DNA with increasing LW, and the difference between pigs from the initial protein treatments progressively diminished and was no longer apparent at 60 kg LW.

5. At 30 kg LW, pigs given the LP diets before 15 kg LW contained less DNA in the subcutaneous adipose tissue from the shoulder joint (P < 0.01) and had larger fat cells (P < 0.05) than pigs given the HP diets initially. However, adipose DNA and fat cell size increased with increasing LW and the differences resulting from the initial protein treatments progressively diminished. On the LE and HE treatments subsequent to 15 kg these differences were no longer evident at 45 and 60 kg respectively.

6. Pigs given the HE intake subsequent to 15 kg, contained less DNA in muscle tissue (P < 0·05) at 60 and 75 kg LW and had larger fat cells (P < 0·05) at 45, 60 and 75 kg LW, than pigs on the LE treatment.

1. The effects of level of feeding and level of protein in the early postnatal period on the cellularity of subcutaneous adipose tissue and body fat content of pigs were investigated in two experiments.

2. In Expt 1, piglets were given a common liquid diet at energy intakes equivalent to 2·8 or 5·2 times energy for maintenance (M) between 1·8 and 6·5 kg live weight (LW), and a common dry diet at 2·8 or 4·5 M between 6·5 and 20 kg LW. Between 20 and 75 kg LW all pigs were given a second dry diet at 4·0 M.

3. In both experiments the effects of nutritional treatments on fat cell number at 20 and 75 kg LW (Expt 1) and at 45 kg LW (Expt 2) were assessed by measuring the DNA content of the subcutaneous adipose tissue contained in the left shoulder joint. Fat cell size was assessed in the same tissue by measuring the diameter of collagenase-released adipocytes.

4. In Expt 1, raising the level of feeding between 1·8 and 6·5 kg LW increased body fat content and average fat cell diameter at both 6·5 (P < 0·01) and 20 kg LW (P < 0·05) but had no effect on either measurement at 75 kg LW. Similarly, raising the level of feeding between 6·5 and 20 kg LW increased body fat content and fat cell size at both 20 (P < 0·01) and 75 kg LW (P < 0·05). There was an almost twofold increase in the DNA content of subcutaneous adipose tisuue between 20 and 75 kg LW. However, it was not significantly affected at either weight by level of feeding before or subsequent to 6·5 kg LW.

5. In Expt 2, reducing the level of dietary protein between 1·8 and 6·5 kg LW increased body fat content (P < 0·01) and fat cell size (P < 0·01) at the latter weight. Although level of dietary protein to 6·5 kg LW had no effect on body fat content or the weight of subcutaneous adipose tissue in the shoulder joint at 45 kg LW, pigs given the lowest-protein diet contained less DNA (P < 0·05) in the subcutaneous adipose tissue and had larger (P < 0·05) fat cells than those given the highest-protein diet to 6·5 kg LW. Reducing the protein content of the diet fed subsequent to 6·5 kg LW increased the body fat content (P < 0·01) and fat cell size (P < 0·01) at 45 kg LW.

1. Six wether sheep were each provided with a permanent cannula in the rumen and re-entrant cannulas in the proximal duodenum.

2. In a preliminary study, the sheep consumed 200 g hay and 400 g concentrates supplemented with up to 40 g linseed oil, coconut oil or cod-liver oil daily. Feed was refused at higher levels of supplementation.

3. Five of the sheep were used in a 5 × 5 Latin-square experiment. They were given 200 g hay and 400 g concentrates alone (B) or supplemented with 40 g linseed oil (L), coconut oil (C), protected linseed oil or protected coconut oil daily. The protected oils were prepared by emulsifying the free oils with formaldehyde-treated sodium caseinate. Formaldehyde-treated sodium caseinate was also included in the other three diets.

4. Digestion in the stomach was measured by spot sampling duodenal digesta, using chromic oxide-impregnated paper as the marker. Microbial flow at the duodenum was measured by use of both diaminopimelic acid (DAPA) and RNA as microbial markers.

5. Both the free oils had broadly similar effects despite their very different fatty acid compositions. Digestion in the stomach of organic matter (OM) was reduced from 0·48 (diet B) to 0·29 (diets L and C) and that of neutral-detergent fibre from 0·50 (diet B) to 0·19 (diet L) and 0·12 (diet C). The molar proportions of acetic acid and n-butyric acid were decreased and that of propionic acid was increased. Protozoal numbers were reduced by 78% (diet L) and 90% (diet C). The flow of total nitrogen and microbial N was increased by both oils and the efficiency of microbial protein synthesis (g N/kg OM apparently digested in the rumen) was increased from 30 (diet B) to 85 (diet L) and 74 (diet C) when based on DAPA and from 41 (diet B) to 94 (diet L) and 81 (diet C) when based on RNA. The efficiency when based on true digestion of OM (g N/kg OM truly digested in the rumen) was increased from 23 (diet B) to 46 (diet L) and 44 (diet C) when based on DAPA and from 29 (diet B) to 49 (diet L) and 46 (diet C) when based on RNA. The amounts of microbial OM (g/d) at the duodenum were increased from 68 (diet B) to 124 (diet L) and 106 (diet C) when based on DAPA and from 92 (diet B) to 136 (diet L) and 115 (diet C, non-significant) when based on RNA.

6. When the oils were given in the protected form, the effects on digestion in the stomach were reduced but not eliminated. No significant increases in the amount of total N or microbial N at the duodenum were established, though there was a tendency for an increase in the efficiency of microbial protein synthesis with protected linseed oil. The results suggested that the method of protection used reduced the effects of the oils on rumen digestion and synthesis but was only partially successful in preventing hydrogenation of the fatty acids.

7. It is concluded that free oils can markedly increase the efficiency of microbial protein synthesis, possibly by their defaunating effect, and that this may enhance the potential for using non-protein-N on oil-supplemented diets.

1. Steers fitted with simple rumen, abomasal and sometimes duodenal cannulas were given isonitrogenous and isoenergetic diets consisting of pellets containing equal amounts of rolled barley and chopped straw together with tapioca alone (B), or with some tapioca replaced by coarse soya-bean meal (M) or finely ground soya-bean flour (F). Diet B had an estimated rumen degradable nitrogen (RDN): metabolizable energy (ME) value of approximately 0·8 g/MJ. The corresponding value for each of the supplemented diets was 1·3–1·4. Diets were given at two levels of intake designed respectively to provide ME intakes to support weight gains of 0·5 kg/d (L) and 1·0 kg/d (H). Chromic oxide and polyethylene glycol were given as indigestible markers. Values were calculated for flows (g/24 h) at the abomasum of organic matter (OM), non-ammonia-N (NAN) and microbial (bacterial)-N (MN). Estimates of MN were based on RNA and α-ε;-diaminopimelic acid (DAP) measurements. The steers had low rumen protozoal counts throughout the whole experiment with fewer than 8000 ciliate protozoa/ml of rumen fluid.

2. Proportions of OM apparently digested between the mouth and abomasum were significantly lower for H than for L intakes but showed no other significant differences. Mean estimated efficiency of microbial protein synthesis was approximately 17 g N/kg OM apparently digested in the rumen for the LB diet, but was significantly greater at approximately 26 g N/kg OM apparently digested for the HB diet. The protein-supplemented diets gave values of 31–32 which were significantly greater than the value for the LB but not the HB diet.

3. Amounts of feed nitrogenous constituents surviving between the mouth and the abomasum were estimated from NAN minus MN corrected for endogenous N. Values for the proportions of feed N degraded, derived from these estimates, were 0·71, 0·66, 0·72, 0·69, 0·67 and 0·70 for diets LB, HB, LM, HM, LF and HF respectively. There were no significant differences due to level of feeding, supplementary protein or the physical form of that protein.

4. Estimates of MN flows at the abomasum based on RNA determinations in fresh samples did not differ significantly from estimates based on DAP determinations. However, storage of aqueous suspensions of mixed rumen bacteria by deep-freezing or freeze-drying resulted in significant losses of RNA. No such losses were observed for abomasal digesta. This meant that if samples were stored by these means before analysis, the use of RNA as a microbial marker was vitiated.

5. In some experiments digesta samples were taken from the duodenum as well as the abomasum. Estimates of total N flows did not differ significantly between these sites.

1. Sheep fitted with rumen and re-entrant duodenal cannulas were given diets of approximately 200 g hay and 400 g concentrate mixture alone, or supplemented daily with 40 g linseed or coconut oils free or protected with formaldehyde-casein in a 5 × 5 Latin-square arrangement. Chromic oxide paper was given as a marker at feeding time and passage to the duodenum of neutral-detergent fibre (NDF) and different sugars were estimated from the values for c0nstituent:marker at the duodenum. Contributions of microbial carbohydrates to these flows were estimated from amounts of RNA present.

2. The carbohydrate composition of mixed rumen bacteria from sheep rumen digesta were similar regardless of diet. Of the sugars entering the duodenum all the rhamnose and ribose and 0·51, 0·24 and 0·35 of the mannose, galactose and starch-glucose respectively, were contributed by the microbes. Virtually all the arabinose, xylose and cellulose-glucose were contributed by the diet.

3. For sheep receiving the basal ration, coefficients of digestibility between mouth and duodenum, corrected where necessary for microbial contribution, were 095,0·66,0·67,0·62,0·45 and 0·51 for starch-glucose, mannose, arabinose, galactose, xylose and cellulose-glucose respectively. Corresponding values when free-oil-supplemented diets were given were 0·95,035,0·38,0·55,0·01 and –0·02 respectively. Values for diets supplemented with linseed oil or coconut oil did not differ significantly. Addition of protected oils to the basal feed also resulted in depressed digestibilities of dietary structural sugars but to a far lesser extent than those observed with the free oils.

4. Apparent digestibility of NDF was altered in the same direction as those of the main structural sugars, averaging 0·50,0· 17 and 0·29 in animals receiving the basal, free-oil-supplemented or protected-oil-supplemented diets respectively. The reasons for the difference between NDF and discrete carbohydrate analytical totals are discussed.

1. The incorporation of uniformly-labelled [14C]glucose into fatty acids and glycogen of adipose tissue and liver was used to assess the effects of zinc deficiency on glucose metabolism in meal-fed rats.

2. Throughout the study, identical feeding regimens were maintained between each of the Zn-deficient groups and their appropriate controls. The feeding regimens were either meal-feeding or ad lib. feeding.

3. Zn deficiency reduced [14C]glucose incorporation into fatty acids of epididymal fat pads of meal-fed rats by 75% when compared with meal-fed controls.

4. Zn deficiency caused a slight but significant decrease in [14C]glucose incorporation into liver fatty acids of meal-fed fats when compared with meal-fed controls.

5. Zn deficiency significantly increased [14C]glucose incorporation into liver glycogen of meal-fed rats in Expt. 2 but not in Expt 1.

6. Some effects of Zn deficiency on glucose metabolism were shown to be independent of the feeding regimen when a single daily meal was given to both Zn deficient and control groups. This method of feeding may be a useful approach to study the effects of Zn on glucose metabolism in the rat.

1. The over-all and regional metabolism of non-esterified fatty acids (NEFA) was studied using a combination of isotopic and arteriovenous-difference techniques.

2. There was a common linear relationship, whether stearic, palmitic or oleic acids were used as tracer, between the arterial NEFA concentration and the rates of entry and oxidation.

3. Assuming that the tracer used reflected the metabolism of all the NEFA, the total entry rate in fed and fasted pregnant ewes was (mean±SE) 0·44±0·02 and 0·55±0·07 mmol/h per kg body-weight respectively. Oxidation of NEFA contributed (mean±SE) 34±5 and 58±7% to the respiratory carbon dioxide in fed and fasted animals, this accounting for (mean±SE) 46±6 and 59±3% of the respective entry rates.

4. Hind-limb muscle both utilized and produced NEFA. The mean gross fractional extraction (calculated from isotopic uptake) was (mean±SE) 9±1%. Gross utilization of any NEFA and appearance of 14CO2 across the muscle were linearly related to the arterial concentration of tracer fatty acid, irrespective of whether this was oleate or stearate. The amount of 14CO2 appearing was consistent with (mean±SE) 54±8% of the CO2 produced by the hind-limb being derived from NEFA oxidation.

5. Infused NEFA were partly converted to ketone bodies. Uptake and oxidation in the hind-limb of ketones formed in the liver could account for approximately 20% of the 14CO2 apparently produced in muscle from NEFA. Correction for this reduces the proportion of CO2 derived from NEFA to 43%. There was some indication that ketones were also produced from NEFA in the hind-limb.

6. NEFA were not a significant energy source for the gravid uterus.

7. An over-all view of energy sources for the whole animal and for hind-limb muscle in normal and fasted pregnant sheep was presented.

1. The effects of phosphorus deprivation on phytate digestibility, phosphorus utilization and intestinal phytase (EC 3.1.3.8) and alkaline phosphatase (EC 3.1.3.1) in rats were investigated.

2. P deprivation was achieved by giving rats a diet containing 3 g P/kg and resulted in hypophosphataemia, hypercalcaemia, hypercalciuria, and lower levels of P absorbed and retained, and calcium retained.

3. Rats adapted to P deprivation by increasing the digestion of total dietary-P and phytate-P.

4. Levels of intestinal alkaline phosphatase and alkaline phytase were not different between the two treatment groups.

5. P deprivation in the rats given the marginal-P diet may be a result of a lower absorption of total dietary-P or increased absorption of inositol phosphates formed during the enzymic hydrolysis of phytate which are not readily utilized by the rat.

6. These results suggest that intestinal phytase and alkaline phosphatase do not play a role in the adaptive increase in phytate digestibility by rats given marginal-P diets. The adaptation may result from enhanced phytase or alkaline phosphatase synthesis by the gastrointestinal microflora stimulated by a lower level of P in the digesta.

1. Protein synthesis in liver and jejunal mucosa was measured in 19-d-old germ-free (GF) and conventional (CV) chicks fed on a semi-purified casein–gelatin (SCG) diet using a massive-dose single injection of [U-14C]phenylalanine. The effect of subsequent feeding for 9 d either a nitrogen-free (NF) diet or an NF diet supplemented with L-methionine (5 g/kg) and L-arginine hydrochloride (2 g/kg) (MA diet) was investigated in both types of chick.

2. In the liver, apart from the amount of DNA, the values for wet weight, protein, RNA, fractional synthesis rate (FSR) and the amount of protein synthesized were reduced after feeding the NF diet and, to a lesser extent, the MA diet. Except that the total amount of liver DNA was higher in the CV chicks than in their GF counterparts (P < 0·01), no environmental effect was significant. When expressed on a unit body-weight basis, liver weight, protein, RNA and DNA were significantly higher in the CV than in the GF chicks.

3. In the jejunal mucosa, the values for wet weight, protein and RNA tended to be reduced after the NF treatment but increased after the MA treatment. Mucosal DNA and the amount of protein synthesized (μg/mm per d) were significantly reduced after the NF diet but were less affected after the MA diet. Mucosal protein FSR and the amount of protein synthesized per mg RNA were significantly reduced after both dietary treatments. No difference was found among dietary treatments in the amount of protein synthesized per mg DNA in jejunal mucosa. Mucosal DNA was significantly higher in the CV chicks and the reverse was true for mucosal protein: DNA.

4. It was suggested that the increased protein synthesis in jejunal mucosa and possibly in liver on supplementation of an NF diet with methionine and arginine would partly, ifnot completely, account for the N-sparing effect of these amino acids.

5. Although the protein: DNA value was smaller in CV chicks, the FSR and the amount ofprotein synthesized tended to be higher than in their GF counterparts irrespective of nutritional status. This might imply that protein degradation rate is greater in the CV state.

1. Two rumen cannulated steers consuming 5·5 kg air-dry lucerne (Medicago sativa) hay/d given at two-hourly intervals were used to study the kinetics in the rumen of the two particulate markers, 103Ru-labelled Tris-(1,10-phenanthroline) ruthenium II chloride ([103Ru]P) and dysprosium (Dy). Provision of markers was achieved by allowing the steers to eat separatedstems of the hay on to which had been sprayed solutions of the markers.

2. The intake of large-particle (retained by a 3·2 mm mesh screen) dry matter (DM) in boluses and the rumen large-particle pool size measured by emptying the rumen wereused to calculate the turnover rate-constant of this pool (1·02 and 1·19/d for steers A and B respectively).

3. The decline with time of both [103Ru]P and Dy associated with large-particle DM in raft digesta was best described by two-compartmental kinetics. The first compartment apparently reflected a combination of the processes of mixing of labelled particles throughout the rumen contents, physical migration of marker from the labelled hay, and physical breakdown of large particles to small particles.

4. The disappearance with time of [103Ru]P and Dy associated with small particles from the raft, ventral digesta and faeces from 3 to 8 d was well described by a single kinetic compartment with a rate constant similar to that of the second compartment of the large particles from the raft.

5. [103Ru]P was rapidly distributed through both the raft and ventral digesta of the rumen. This observation, taken together with measurements of migration of [103Ru]P, suggested that on entering the rumen much of the [103Ru]P did not remain associated with the original feed material.

6. The majority (63–64%) of Dy entered the raft digesta and mixed only slowly through the rumen contents. Some Dy (18–27%) apparently migrated rapidly from large particles and to small particles immediately after ingestion and there was also evidence for some slow migration from small to large particles.

7. When used under the conditions described for this experiment neither [103Ru]P nor Dy was satisfactory as a marker to trace the passage through the rumen of a particular meal.

1. Absorption of magnesium from the temporarily-isolated, emptied and washed rumen of four 10–12-month-old heifers was measured at five different Mg concentrations (2·5, 5·0, 7·5, 12·5 and 20 mmol/l).

2. Net absorption of Mg was observed at all concentrations. Saturation occurred at a concentration of 12·5 mmol Mg/l.

3. Using an Eadie–Hofstee plot, the Michaelis–Menten constant (Km; 11·43 mmol/l) and maximal efflux (Vmax; 120·3 μmol/min) were estimated.

4. The phenomenon of saturation supports the assumption that Mg transport across the rumen wall of heifers is an active process.

1. The calcium and phosphorus concentrations in foetal tissue or the placental transfer of 45Ca and 32P, or both, were studied in fifty-five control or 1α-hydroxycholecalciferol (1α-(OH)D3)-treated (0·1 μg/kg body-weight per d for 12 d) ewes between 77 and 140 d of gestation.

2. Treatment resulted in a significant increase in the concentration of Ca and P in foetal tissues at all stages of gestation except at 140 d when, it is suggested, foetal mineralization may approach a maximum value.

3. This increase in Ca and P concentration in foetal tissues was associated with an increased placental transfer of Ca, though at 111 and 120 d gestation this increase was not significant. P transfer, which was only measured at 140 d gestation, was also significantly higher in treated animals.

4. The concentrations of Ca and P in both maternal and foetal plasma were increased significantly by the 1α-(OH)D3 treatment.

5. Whereas the concentration of Ca in the plasma of foetuses was always greater than in their dams, the concentration of plasma P in treated animals, unlike controls, was lower in foetuses than dams. This suggests that the increased placental transfer of P, unlike that of Ca, may be a passive rather than an active process.

1. Glucose turnover in fed and 48 h-starved lactating goats was determined during a glucose load of 500 μmol/min using a continuous infusion of [U-14C]- and [3-3H]glucose.

2. Endogenous rates of irreversible glucose turnover (i.e. total rates of irreversible glucose turnover minus the rate of exogenous glucose supply) were depressed during glucose loading by 14 and 62% in the fed and starved animals respectively.

3. Plasma glucose concentrations increased significantly by 57 and 88% in the fed and starved goats respectively. Plasma insulin concentrations increased by 108 and 128% in the fed and starved animals respectively.

4. Milk yields increased significantly (41%) in the starved animals during glucose loading, but were unaffected in fed animals.

5. In both the fed and 48 h-starved goats, mammary glucose metabolism via glycolysis and the pentose phosphate pathway appeared to be stimulated by glucose loading.

1. The rate of blood flow in the portal and hepatic veins, and the net exchange across the gut and liver of volatile fatty acids (VFA), glucose, lactate, pyruvate, amino acids, ketone bodies, glycerol, non-esterified fatty acids (NEFA) and oxygen, were measured in lactating and non-lactating cows (a) in the normal, fed state and (b) before, during and after 6 d of fasting.

2. Blood flow rate through the liver was 52% higher in normal, fed, lactating cows as compared with non-lactating cows, and was decreased by fasting in both groups of cows. Portal blood flow rate increased with an increase in metabolizable energy (ME) intake.

3. Lactating, as compared with non-lactating, cows exhibited lower arterial concentrations of glucose and lactate, higher net portal outputs of VFA and ketone bodies, a higher net hepatic output of glucose, and higher net hepatic uptakes of propionate and lactate. The splanchnic outputs of acetate, glucose and hydroxybutyrate were all apparently greater in the lactating cows.

4. Fasting caused a rapid decrease in the blood concentrations of the VFA and an increase in those of glycerol and NEFA. The portal, i.e. gut, outputs of VFA, lactate, ketone bodies, alanine and (serine+threonine), and the portal uptake of O2, were all decreased by fasting. Fasting for 6 h also decreased the hepatic output of glucose and acetate by 77 and 95% respectively, increased the hepatic uptake of pyruvate, glycerol and NEFA, and doubled hepatic ketone-body output. The splanchnic output of acetate and glucose and the splanchnic uptake of O2 were also decreased by fasting.

5. The net portal outputs of VFA, lactate and hydroxybutyrate, and the net hepatic output of glucose, were all correlated with ME intake in fed and fasted cows. Hepatic glucose output was also correlated with milk yield.

6. The net hepatic uptake of gluconeogenic precursors measured in this study could account for net hepatic glucose output in the fasted cows, but not in the fed cows. The net hepatic uptake of the ketogenic precursors butyrate and NEFA was sufficient to account for the hepatic output of ketone bodies in both fed and fasted cows, but it is unlikely that the hepatic uptake of ketogenic precursors could also account for the observed hepatic output of acetate.

1. In order to exclude the possibility of differences in maternal care which are known to result from typical methods of undernutrition during the suckling period, rat pups were reared artificially on different planes of nutrition away from their mothers.

2. Artificial rearing was accomplished by fitting infant rats with a gastric cannula through which a milk substitute was infused intermittently. Rats were fed thus from 4 to 21 d on a high (ARHI) or a low (ARLO; 44% of ARHI level) plane of nutrition. Underfeeding of the ARLO group was continued till 25 d, after which all rats were given a good-quality pelleted diet ad lib.

3. Compared with mother-reared (MR) litter-mates, ARHI rats showed advanced eye-opening and, at 21 and 25 d, they resisted restraint more strongly.

4. Growth in body-weight of ARHI and MR rats was similar but, when autopsied at 32 weeks, the ARHI rats were shorter (nose–rump length) and had lighter gastrocnemius muscles, adrenals and brains, but heavier epididymal-fat pads.

5. ARLO rats had deficits at 32 weeks compared with ARHI rats in whole body, kidney and epididymal-fat-pad weights, and in tibia length.

6. In a second experiment, ARHI and MR rats were killed at 21 d. All the differences found at 32 weeks were already present at 21 d. In addition, the ARHI pups had enlarged livers and intestines but shorter tibias.

7. The milk substitute, which is one commonly used in such studies, has a low protein and high carbohydrate content compared with rats' milk. This difference probably caused the abnormal organ growth of ARHI rats.