The role of cholecystokinin (CCK) in modulating feed intake depression in parasite-infected lambs was investigated using CCK receptor antagonists (L364–718 and loxiglumide). Four experiments were carried out using ewe lambs infected with 4000 Trichostrongylus colubriformis larvae/d or non-infected controls (n 8, live weight 25 kg). Animals were fed daily on a nutritionally complete pelleted diet and had free access to water. In the first experiment, infected and non-infected animals were injected subcutaneously with CCK antagonist (100 μg L364–718) or carrier alone as a single dose. In the second experiment, CCK antagonist (loxiglumide: 0, 5, 10 or 20mg/kg live weight) was injected into a jugular vein immediately before feeding. In the third experiment, animals were infused continuously with the CCK antagonist (loxiglumide; 10mg/kg per h) for 10 min before feeding and for the first 2 h of feeding. In the final experiment, lambs were fitted with an indwelling cerebral ventricular cannula and infused with a CCK antagonist (loxiglumide, 162μg/min), CCK agonist (CCK-8, 2.5 pmol/min), loxiglumide plus CCK-8 or sterile saline solution alone via the cannula for 30 min before feeding and for the first 60 min of feeding. In all the experiments short-term feed intake was recorded at 10 and 15 min intervals for the first and second hours of feeding respectively, then at hourly intervals for the remainder of the 8 h recording period. Peripheral injection with L364–718 or loxiglumide did not elevate feed intake in either the infected or non-infected animals. However, feed intake was increased (P < 0.05) in the short term by central infusion of loxiglumide, this effect being greater in the infected animals and apparently due to an elevation in intake during the second hour of feeding. CCK-8 depressed short term feed intake only in the infected animals (P < 0.05). Total daily feed consumption was not influenced by any of the pharmacological agents. The results indicate an involvement of central CCK receptors in regulation of feed intake depression following gastrointestinal parasitism of sheep and the possibility of a similar role in non-infected sheep. They do not support the singular importance of a peripheral action of CCK in determining satiety.

Cholecystokinin: Loxiglumide: Feed intake: Gastrointestinal parasites

The aim of the present study was to investigate the relationship of Ca intake and serum Ca levels during the third trimester of pregnancy with levels of the same mineral in transition milk (days 13−14 of lactation) and mature milk (day 40 of lactation). The study subjects were a group of fifty-seven healthy, lactating mothers aged between 18 and 35 years (mean 27 (SD 3·7) years) whose pregnancies and labour were attended by the Department of Obstetrics and Gynaecology of Cuenca INSALUD Hospital, Spain. Ca intake during the third trimester was determined by recording the consumption of foods over a 5 d period and by registering Ca provided by dietary supplements. The same method was used to investigate the intake of protein, vitamin D, fibre and Fe, nutrients that could affect the use of dietary Ca. Ca levels in maternal serum during this stage of pregnancy, during lactation and in transition and mature milk samples, were determined using 2-cresolphthalein complexone. During pregnancy 70·2% of subjects showed Ca intakes below 1100mg/d (75th percentile). The consumption of Ca supplements was very small and hardly modified the mean quantity supplied by the diet. Subjects with an intake < 1100mg/d showed no fall in Ca levels in serum, either during pregnancy or lactation, nor were decreased levels found in transition milk. However, these subjects showed lower Ca levels in mature milk (5·95 (SD 1·56) mmol/1) than did subjects with greater Ca intakes (6·82 (SD 1·31) mmol/1). This may suggest that breast-fed babies of mothers with lower Ca intakes during pregnancy also receive less Ca.

Multi-frequency bioimpedance analysis (MFBIA) was used to determine the impedance, reactance and resistance of 103 lamb carcasses (17·1–34·2 kg) immediately after slaughter and evisceration. Carcasses were halved, frozen and one half subsequently homogenized and analysed for water, crude protein and fat content. Three measures of carcass length were obtained. Diagonal length between the electrodes (right side biceps femoris to left side of neck) explained a greater proportion of the variance in water mass than did estimates of spinal length and was selected for use in the index L2/Z to predict the mass of chemical components in the carcass. Use of impedance (Z) measured at the characteristic frequency (Zc) instead of 50 kHz (Z50) did not improve the power of the model to predict the mass of water, protein or fat in the carcass. While L2/Z50 explained a significant proportion of variation in the masses of body water (r2 0·64), protein (r2 0.34) and fat (r20·35), its inclusion in multi-variate indices offered small or no increases in predictive capacity when hot carcass weight (HCW) and a measure of rib fat-depth (GR) were present in the model. Optimized equations were able to account for 65–90% of the variance observed in the weight of chemical components in the carcass. It is concluded that single frequency impedance data do not provide better prediction of carcass composition than can be obtained from measures of HCW and GR. Indices of intracellular water mass derived from impedance at zero frequency and the characteristic frequency explained a similar proportion of the variance in carcass protein mass as did the index L2/Z50.

Within the overall objective of whether ruminants are able to form conditioned aversions (CFA) toward a food flavour associated with the administration of an aversive stimulus which occurs naturally in food plants (oxalic acid, OA), two specific objectives were tested: (1) whether the rate and degree of formation of CFA are dependent on the dose rate of OA administered and (2) whether the persistence of formed CFA depends on the previous dose rate of OA. Sheep were conditioned to associate the specific flavour of one of two novel foods with either the oral administration of OA or equivalent placebos. Four dose rates of OA were tested (0.06, 0.12, 0.18 and 0.24 g/kg sheep live weight per d), with twelve sheep per dose. Each conditioning period lasted for 8 d and was repeated four times. At the end of each conditioning period the preference for the two flavours was measured in short-term, 20min preference tests. The persistence of the CFA was measured at 0, 7, 21 and 49 d after the completion of the conditioning phase with long-term, 3 h preference tests. The results of the experiment indicated that: (1) the rate and degree of formation of CFA were dependent on the rate of administration of OA; (2) sheep required repeated exposures to the lower dose rates of OA in order to develop CFA and these CFA did not persist in the absence of continual reinforcement; (3) CFA to the higher dose rates of OA were developed after as little as one exposure and persisted over a period of at least 7 weeks. These findings are consistent with the expectation that ruminants should be able to select a diet which minimizes the risk of consumption of potentially harmful foods, whilst at the same time maintaining a degree of flexibility in their feeding behaviour.

The effect of dietary intake level on in vivo plasma leucine and plasma palmitate flux rates and on the response to a bolus injection of bovine growth hormone (GH) was investigated in six young steers. Animals were fed on a pelleted diet of dried grass–barley (0.7:0.3, w/w) in quantities sufficient to supply 0.8, 1.2, 1.6, 2.0, 2.4 or 2.65 × maintenance energy requirement, offered in hourly portions. Continuous intravenous infusions of [1-13C]leucine or [1-13C]palmi-tate were used to determine the flux of amino acid and fatty acid through the plasma pool before, immediately (1–3 h) after and 22–24 h after a subcutaneous injection of bovine GH (0.55 mg/kg body weight). Hourly blood samples were taken for 27 h to monitor the temporal responses of circulating hormones and metabolites following GH administration. The animal on the lowest plane of nutrition had elevated plasma GH and reduced insulin-like growth factor-1 concentrations compared with those fed on higher intake levels. Plasma leucine flux and leucine concentration increased with intake while palmitate flux and plasma non-esterified fatty acid (NEFA) concentrations were inversely related to intake. Leucine flux rate decreased in the animals fed on the two highest intake levels in response to GH 22–24 h after administration, but plasma leucine concentrations were reduced in all animals at this time. Only the animal fed on the lowest intake level showed an immediate response to GH (within 3 h of administration) with increased palmitate flux and plasma NEFA concentrations but a lipolytic response was apparent in other animals 22–24 h post-administration although the magnitude of the response was markedly reduced at high intakes. We conclude that lipid and protein metabolism are differentially responsive to GH and nutritional status.

Three experiments were carried out to establish a response model between intake and urinary excretion of purine compounds. In Expt 1 the relationship between the intake of purine bases (PB) and the excretion of total purine derivatives (PD) was determined in seven growing rabbits with a mean initial live weight (LW) of 2·03 (SE 0·185) kg, aged 70 d, each fitted with a wooden neck collar to prevent caecotrophagy. They were fed on five experimental diets formulated with different levels of nucleic acids (0·00, 3·75, 7·50, 11·25, 15·00 g yeast-RNA/kg diet). The relationship between intake of purine (x, μmol/kg W0·75) and total urinary PD excretion (y, μmol/kg W0·75), y = 0·56 + 0·67x (r2 0·86; RSD 0·338), indicated that about 70% of duodenal PB were recovered as urinary PD and that the endogenous contribution was constant and independent of dietary PB supply. Endogenous excretion of PD (allantoin and uric acid) was measured in a second experiment using six rabbits fed on a purine-free diet and fitted with neck collars to avoid caecotrophagy. Basal daily urinary excretion values for allantoin and uric acid were 532 (SE 33·9) and 55 (SE 7·3) μmol/kg W0·75 respectively; xanthine and hypoxanthine were not found in urine samples and therefore the sum of allantoin and uric acid should comprise the total excretion of PD (588 (SE 40·1) μmol/kg W0·75). The xanthine oxidase (EC 1·2.3·2) activity in plasma, liver, duodenum, jejunum and kidney was measured in a third experiment. The activities of xanthine oxidase in duodenal and jejunal mucosa, liver and kidney were: 0·61 (SE 0·095), 0·37 (SE 0·045), 0·035 (SE 0·001) and 0 units/g fresh tissue respectively and in plasma 2·96 (SE 0·094) units/1. The results show that urinary excretion of PD may be a useful tool to estimate duodenal PB input and microbial protein intake once the relationship between PB and N has been established in caecal micro-organisms.

A total of sixty-five observations on heat production during fasting and physical activity were obtained in four groups of pigs differing in breed and/or castration (Meishan (MC) and Large White (LWC) castrates and Large White (LWM) and Piétrain (PM) males) with body weight (BW) ranging between 25 and 60 kg. Pigs were fed ad libitum before fasting. Heat production was measured using indirect calorimetry. Fasting heat production (FHP) was proportional to the body weight raised to the power 0.55, but with group-specific proportionality parameters (810, 1200, 1220 and 1120kJ/kg BW0.55 per d for MC, LWC, LWM and PM respectively). Group effects could be removed by expressing FHP as a function of muscle, viscera and fat: FHP (kJ/d) = 457(muscle)0.81 + 1969(viscera)0.81 - 644(fat)0.81. It is hypothesized that different breeds with equal muscle and visceral mass, can have different FHP. The negative coefficient for fat would then be the result of a low FHP rather than a cause of it. Because a large part of the variation in tissue composition between groups was due to MC group, a separate equation for the lean groups was established. For lean pigs, FHP could be expressed as a function of muscle and viscera alone: FHP (kJ/d) = 508(muscle)0.66 + 2011(viscera)0.66. Both type of pig and BW affected the number of bouts of physical activities (i.e. standing or sitting) per day, the duration of activity and the total cost of activity. Energetic cost of activity was proportional to the muscle mass raised to the power 0.91 (FHPactivity (kJ/h activity) = 21.0(muscle)0.91). Physical activity represented less than 10% of the total heat production in fasting growing pigs housed alone in metabolic cages and kept in a quiet environment.

Effects of dietary protein restriction and ovariectomy on plasma concentrations and hepatic messenger RNA (mRNA) of insulin-like growth factor-I (IGF-I) and insulin-like growth factor binding proteins (IGFBP) were investigated in young female rats. Ovariectomy increased plasma IGF-I concentration in rats fed on either a 50 g casein/kg diet (protein-restricted diet) or a 200 g casein/kg diet (control diet), but it increased IGF-I mRNA in liver only in the rats fed on the control diet. On the other hand, by Western ligand blot analysis, we observed that ovariectomy increased plasma IGFBP-3 concentration, and decreased plasma IGFBP-4 concentration. Ovariectomy did not affect IGFBP-1 and IGFBP-2 mRNA in liver, but dietary protein restriction significantly increased them, which may correspond to their plasma concentrations. The present results show that ovarian hormones and dietary protein content affect the plasma concentrations of IGF-I, IGFBP-3 and IGFBP-4 and hepatic mRNA of IGF-I, IGFBP-1, IGFBP-2, IGFBP-3 and IGFBP-4 in different manners.

Previous studies have described high plasma triiodothyronine (T3) concentrations and sympathetic activity in rats fed on low-protein diets. The present investigation examined how the nutritional status of rats fed on a low-protein diet was affected when these hormonal changes were reduced by drug administration. The low-protein diet (LP group) prevented growth, reduced plasma albumin levels, elevated plasma T3 concentration, and increased both the weight of the interscapular brown adipose tissue (BAT) and the activity of BAT cytochrome c oxidase (EC 1.9.3.1). Lowering the plasma T3 concentration (with carbimazole; CA group) elevated the plasma insulin concentration, promoted a small increase in the plasma albumin concentration and caused weight gain in comparison with the LP group. Reduction of sympathetic activity (with α-methyl-p-tyrosine; MT group) promoted a small elevation in plasma albumin concentration accompanied by a diminished T3 concentration, BAT weight, and an increase in fat deposition in relation to LP rats. In a second experiment, simultaneous lowering of the plasma T3 concentration and sympathetic activity (CA/MT group) resulted in weight gain associated with elevated plasma insulin concentration and fat deposition and a marked reduction in BAT cytochrome c oxidase activity. However no change in the hypoalbuminaemia was observed. The results of the present study suggest that in spite of the previously described increase in metabolic rate in rats fed on a diet with low-protein concentration when compared with controls, the mechanisms involved in the control of BAT activity and fat deposition seem to be independent of those which cause liver protein depletion and hypoalbuminaemia.

The proper use of a time-dependent and controlled nutrition regimen during the hormone-sensitive growth phase before first parturition can significantly affect mammary growth and subsequent lactation performance. The objective of the present study was to determine if a compensatory nutrition regimen improves lactation performance by affecting proliferation and apoptosis of mammary epithelial cells. Forty female rats (7 weeks of age, average weight 148 g) were assigned to either (1) control, free access to diet or (2) stair-step compensatory nutrition regimen, an alternating 3–4-week schedule beginning with an energy-restricted diet (31·2% restriction) for 3 weeks, followed by the control diet for 4 weeks. Estimated milk yield was greater (P <0·05) on day 15 of lactation in the compensatory nutrition group than in the control group. Mammary cell proliferation values were 1·4- and 2·7-fold greater in mammary tissue from the compensatory group during pregnant and early lactating stages respectively, compared with those from the control group. Ornithine decarboxylase (EC 4.1.1.17)mRNA was 24% higher (P <0·05) in mammary tissues of rats from the compensatory nutrition group during pregnancy than in those from the control group. These results indicate that the compensatory nutrition regimen imposed during the peripubertal growth phase stimulated mammary epithelial cell proliferation and improved lactation performance.

Differences between the fermentation characteristics of cell contents (CC) and protease-treated cell walls (CW) of young leaves of Italian ryegrass (Lolium multiflorum Lam.) cultivar Multimo (tetraploid), were studied in vitro. Gas and volatile fatty acid (VFA) production rates were measured at regular intervals, as was the degradability of organic matter (OM) of CW. The measured VFA were used to predict the gas production and fermentable OM using stoichiometric calculations. For CW the volume and kinetics of measured gas production were the same as those predicted from the VFA formed. In contrast, the measured gas production for CC was consistently less than predicted, indicating that the stoichiometric equations were not valid for rapidly fermenting substrates. For both CC and CW, the relative rate of acetic acid production levelled off more slowly than for other VFA, resulting in an increasing gas yield (in ml/g fermentable OM) after 12 (CW)-24 (CC)h incubation. Consequently, the fermentation of OM was not linearly related to gas production kinetics. For CW, the kinetics of decline of degradable OM and fermentable OM were the same, after correction for a constant ‘lost fraction’ of degradable OM of 205 g/kg OM. This work indicates the value of detailed studies of fermentation processes to evaluate herbage quality. In particular, the role of CC and the difference between degradation and fermentation require further attention.

Four preruminant calves with implanted electrodes in the duodenum and a catheter in the external jugular vein were used for investigation of plasma gut regulatory peptide profiles during different phases of migrating myoelectric complex (MMC) in the small intestine. The effects of different dietary proteins on the rhythmic activity of gut peptides and gastrointestinal motility were compared. In particular, the effects of skimmed-milk protein (retaining physiological patterns of abomasal clotting, and abomaso-intestinal digesta flow) v. fish protein (devoid of clotting activity and modifying the digesta flow) were studied. In calves fed on the milk diet, plasma concentrations of pancreatic polypeptide, motilin, secretin, cholecystokinin (CCK) and somatostatin, but not vasoactive intestinal polypeptide or gastrin, fluctuated in phase with the duodenal MMC in the preprandial period. Feeding transiently affected the intestinal MMC and abolished the peptide fluctuations in a specimen-specific manner. In contrast, calves fed on the fish-protein diet showed more profound changes in intestinal MMC. In these animals the MMC-related fluctuations were significant only for plasma CCK. In conclusion, the source of dietary protein has an impact on the physiological endocrine function of the small intestine. Observed fluctuations of plasma gut regulatory peptides seem to be secondary to duodenal motility cycles.

To reassess the hypothesis that fatty acid catabolism occurs to completion via β-oxidation, male Sprague–Dawley rats receiving continuous total parenteral nutrition (TPN) including 43% energy as fat were infused with [1-13C]- or [8-13C]triolein. Expired CO2 was collected continuously for 4 h and its 13C: 12C ratio determined by isotope–ratio mass spectrometry. Bicarbonate retention was also assessed over 4 h by infusion of NaH14CO3 and measurement of the expired 14CO2. A possible loss of label from [8-13C]oleic acid from the citric acid cycle via labelled acetyl-CoA without oxidation to CO2 was assessed by infusing further animals with acetate labelled with 14C either at C atoms 1 or 2 and determination of its conversion to expired 14CO2. At isotopic steady state, 63.2 (SE 1.6)% (n 8) of the infused [1-14C]acetate and 46.0 (SE 1.2)% (n 8) of [2-14C]acetate was recovered as expired 14CO2. After correction for bicarbonate retention and non-oxidative isotope loss, 37.3 (SE 1.2)% (n 20) of the [1-13C]triolein was found to have been oxidized, whereas 32.6 (SE 1.0)% (n 20) of the [8-13C]triolein was oxidized (P ≤ 0.01). The lower oxidation of the C atom at position 8 of oleic acid than that at position 1 indicates incomplete oxidative breakdown of the fatty acid after entering β-oxidation.

Alternative models for analyses of liver and mammary transorgan data were formulated and fitted to liver and mammary data sets respectively. The models considered metabolite inputs to and effluxes from an extracellular pool. In general, fits were greatly improved over previous efforts using other models (Miller et al. 1991a; Hanigan et al. 1992; Wray-Cahen et al. 1997). Errors of prediction were generally less than 15% for liver and less than 20% for mammary glands. With the possible exception of glutamine for the udder, all metabolites exhibited linear responses to extracellular concentrations within the observed ranges of inputs. However, prediction biases were evident for β-hydroxybutyrate, acetate, and propionate by liver and for arginine, histidine, citrulline and glycerol by mammary tissue. These biases were hypothesized to be caused by the existence of additional regulatory complexity. With the exception of histidine, parameter estimates for essential amino acid removal by liver were 2–3-fold lower than for mammary gland. Infusion of an amino acid mixture into the mesenteric vein did not alter parameter estimates for removal of amino acids by the liver. Treatment of cows with bovine somatotropin resulted in changes in mammary parameter estimates for aspartate, glutamate, leucine, phenylalanine, glucose, and glycerol.

The effect of feeding live Lactobacillus reuteri cells containing active bile salt hydrolase (BSH) on plasma cholesterol levels was studied in pigs. During an experiment lasting 13 weeks, twenty pigs were fed on a high-fat, high-cholesterol, low-fibre diet for the first 10 weeks, and a regular pig diet for the last 3 weeks. One group of animals received, twice daily, 11·25 (SD 0·16) log10 colony forming units of the potential probiotic bacteria for 4 weeks (from week 3 until week 7). From week 8 onwards, the treated group was again fed on the same diet as the control group without additions. The total faecal Lactobacillus counts were only significantly higher in the treated pigs during the first 2 weeks of L. reuteri feeding. Based on limited data, it was suggested that the administered Lactobacillus species had caused a temporary shift within the indigenous Lactobacillus population rather than permanently colonizing the intestinal tract. The probiotic feeding brought about significant lowering (P ≤ 0·05) of total and LDL-cholesterol concentrations in the treated pigs compared with the control pigs, while no change in HDL-cholesterol concentration was observed. The data for faecal output of neutral sterols and bile salts were highly variable between the animals of each group, yet they indicated an increased output in the treated pigs. Although the blood cholesterol levels went up in both groups during the 3 weeks following the Lactobacillus administration period, significantly lower serum total and LDL-cholesterol levels were observed in the treated pigs. During the final 3 weeks of normalization to the regular diet, cholesterol concentrations significantly decreased in both animal groups and the differences in total and LDL-cholesterol concentrations between the groups largely disappeared.

We investigated the effect of oral high-dose cholecalciferol on plasma and adipose tissue cholecalciferol and its subsequent release, and on plasma 25-hydroxyvitamin D (25(OH)D). Female Wistar rats (n 126) received 37·5 μg cholecalciferol/d for 14 d and were subsequently studied for a further 88 d. Two subgroups of eighteen rats each were fasted for 3 d immediately after treatment (days 14−17) and at the end of the study (days 98−101). During treatment, plasma cholecalciferol increased rapidly to reach a steady-state. Plasma 25(OH)D and adipose tissue cholecalciferol increased linearly for 1 - 2 d after treatment. Serum Ca and inorganic phosphate also increased. Subsequently half-lives of plasma cholecalciferol and 25(OH)D, and perirenal and subcutaneous adipose tissue were: 1·4, 22·5, 97·5 and 80·9 d respectively. Fasting, as compared with ad libitum feeding, caused increased plasma free fatty acids, weight loss up to 14% and increased adipose tissue cholecalciferol (nmol/g wet weight). It did not affect plasma cholecalciferol immediately after cholecalciferol treatment, but raised plasma 25(OH)D. Fasting at the end of the study decreased plasma cholecalciferol and increased plasma 25(OH)D. We conclude that orally-administered cholecalciferol rapidly accumulates in adipose tissue and that it is very slowly released while there is energy balance. Fasting causes preferential loss of triacylglycerols from adipose tissue, as opposed to cholecalciferol, but nevertheless augments plasma 25(OH)D. Adipose tissue may act as a ‘buffer to functional vitamin D status’ by preventing, to a certain extent, unregulated production of 25(OH)D from dietary vitamin D, and by slowly releasing vitamin D under fasting conditions.

This study was carried out to analyse glucocorticoid-induced muscle wasting and subsequent recovery in adult (6-8 months) and old (18-24 months) rats because the increased incidence of various disease states results in hypersecretion of glucocorticoids in ageing. Adult and old rats received dexamethasone in their drinking water for 5 or 6 d and were then allowed to recover for 3 or 7 d. As dexamethasone decreased food intake, all groups were pair-fed to dexamethasonetreated old rats (i.e. the group that had the lowest food intake). At the end of the treatment, adult and old rats showed significant increases in blood glucose and plasma insulin concentrations. This increase disappeared during the recovery period. Protein synthesis of different muscles was assessed in vivo by a flooding dose of [13C]valine injected subcutaneously 50 min before slaughter. Dexamethasone induced a significant decrease in protein synthesis in fast-twitch glycolytic and oxidative glycolytic muscles (gastrocnemius, tibialis anterior, extensor digitorum longus). The treatment affected mostly ribosomal efficiency. Adult dexamethasone-treated rats showed an increase in protein synthesis compared with their pair-fed controls during the recovery period whereas old rats did not. Dexamethasone also significantly decreased protein synthesis in the predominantly oxidative soleus muscle but only in old rats, and increased protein synthesis in the heart of adult but not of old rats. Thus, in skeletal muscle, the catabolic effect of dexamethasone is maintained or amplified during ageing whereas the anabolic effect in heart is depressed. These results are consistent with muscle atrophy occurring with ageing.

The effect of high- (hePE) and low- (lePE) esterification pectin and high- (hvGG) and low-(lvGG) viscosity guar gum on plasma, hepatic and biliary lipids and on prevention of cholesterol gallstones was investigated in male golden Syrian hamsters (Mesocricetus auratus). Hamsters were fed on cholesterol-rich (4g/kg), gallstone-inducing diets for 6 weeks. The diets were supplemented with 80g hePE, lePE, hvGG or lvGG/kg or 80g additional cellulose/kg. No significant differences in plasma total cholesterol and triacylglycerol concentrations between hvGG and lvGG and the gallstone-inducing or cellulose-enriched diets were observed. The hePE diet produced a 16% (non-significant) reduction in total plasma cholesterol but significantly decreased the plasma triacylglycerol level by 45%. The lePE diet caused only minor changes in plasma lipids. Hepatic cholesterol concentrations were significantly higher in hamsters fed on hvGG, lvGG, hePE or lePE primarily due to the accumulation of esterified cholesterol. Supersaturated bile samples, with lithogenic indices ranging from 1.6 to 2.0, were determined with all diets. The hePE and lePE diets slightly altered the bile acid profile by increasing glycocholic acid and decreasing taurochenodeoxycholic acid concentrations resulting in a higher cholic: chenodeoxycholic acid ratio. Cholesterol gallstone formation was not substantially inhibited by the two varieties of pectin and guar gum. The hvGG, lvGG, hePE and lePE diets did not alter faecal weight and caused only minor increases in faecal bile acid excretion. In general, the present findings demonstrate that dietary pectins and guar gums had only minor effects on cholesterol metabolism and did not prevent cholesterol gallstone formation in this hamster model. Possible explanations for this lack of a distinct response to pectin and guar gum are discussed.

The effect of intake on urea production, entry into the digestive tract and return of N to the ornithine cycle was studied in four sheep. Each sheep received 0–6, 1–2 and 1.8 × estimated maintenance energy intake quantities of grass pellets for 9 d. After 4 d of adjustment, N balance measurements were conducted between days 5 and 8. From day 7 to day 9 animals were continuously infused, via the jugular vein, with [15N15N]urea and three urine samples were collected at approximately 2h intervals 48–54h after the start of infusion. Total urea and enrichments of [15N15N]- and [14N15N]urea in the urine samples were determined. Urea production was calculated from the isotopic dilution of [15N15N]urea and entry into the gastrointestinal tract (GIT) obtained from the difference between this and urinary urea elimination. Urea which enters the GIT undergoes hydrolysis to liberate NH3 which may be reabsorbed and enter the ornithine cycle, in which case the product is [14N15N]urea, based on the probabilities of labelled and unlabelled N providing ureagenic precursors. The quantity of urea-N which returns to the ornithine cycle from the GIT can thus be calculated. Existing models based on this approach yield overestimates of the fate of individual urea molecules due to a failure to allow for multiple recycling of [14N15N]urea species through the GIT. Refinements introduced to cover this resulted in a 33–48 % reduction in calculated return of label for the current study. The present model also predicted that 95 % of the label movements across the GIT could be accommodated by three or fewer entries and returns of urea-N and 99 % by recycling for a maximum of six occasions. Urea-N production increased with intake (P < 0.001) and exceeded digestible N values at all intakes. Urea which entered the digestive tract, both in absolute terms (P < 0.001) and as a proportion of production (0.62, 0.69, 0.73; P = 0.027), increased with intake. The proportion of entry into the digestive tract which was returned to the ornithine cycle remained reasonably constant (0.37–0.41) across all intakes but the absolute amount increased (5.6, 9.2 and 15.0gN/d; P < 0.001) with intake. If allowance is included for losses of 15N in faeces then the approach offers a relatively simple means of estimating anabolic reuse of urea by digestive tract micro-organisms and can complement data obtained from the technically more demanding arterio-venous and multiple-isotope techniques used hitherto.

Urea: Gastrointestinal tract: [15N]kinetics: Sheep