To investigate changes in the thermic effect of a meal (TEM) during pregnancy, metabolic rate was measured in the fasting state and during the first 180 min after consumption of a standardized test meal in twenty-seven women before, and in each trimester of pregnancy. Resting metabolic rate (RMR) showed a steady increase over pregnancy: values in weeks 24 and 35 of pregnancy were significantly higher than the prepregnancy baseline (Tukey's studentized range test). The pattern of changes of postprandial metabolic rate (PPMR) was similar to that of RMR. Consequently TEM, calculated as PPMR minus RMR, did not change over pregnancy; mean TEM values (kJ/180 min) before and in weeks 13, 24 and 35 of pregnancy were 117 3 (sd 19.4), 116.4 (sd 23.7), 111.6 (sd 24.4) and 111.5 (sd 26.7) respectively. We consider changes in TEM of less than 15% to be of little importance physiologically. If true changes in TEM over pregnancy are 15 % or more we would have had a 90 % chance of observing significant changes in TEM in the present study, given the number of subjects and the methods used. Therefore, we conclude that no substantial reduction in TEM occurs during pregnancy.

The present study focuses on the digestion and absorption of milk and fermented milk (FM) reflected by gastro-ileal N and electrolyte movements in six healthy volunteers. The N and electrolyte content of the intestinal effluents were analysed both at the beginning of the jejunum and in the distal ileum. The gastric half-emptying time of the liquid phase was significantly (P < 0·05) shorter for milk (35 (SE 2) min) than for FM (60 (SE 2) min). The N balance showed that 58 and 50 % of ingested proteins, milk and FM respectively were absorbed between the stomach and the proximal jejunum and that 91 and 90% respectively were absorbed between the stomach and the terminal ileum in 240 min. Evaluation of mineral absorption indicated that 44 and 67% of Ca was absorbed in the duodenum after milk and FM ingestion respectively, and 41 and 11% of Ca disappeared between the jejunum and the ileum respectively. With regards to N and Ca intestinal availability, the present study confirms that FM products represent an interesting source of N as well as minerals for man. This confers on FM a beneficial effect compared with milk especially for lactase (EC 3.2.1. 108)–deficient subjects and children with persistent diarrhoea.

Cardiac output (CO; indirect Fick), blood pressure (BP) and heart rate (HR; oscillometry), superior mesenteric artery blood flow (SMABF; Duplex Doppler) and calf blood flow (CBF; venous occlusion plethysmography) were recorded in the fasted state and for 120 min following the ingestion of 1, 2, and 3 MJ, high-carbohydrate meals in eight healthy females. BP was unchanged following food. HR (P < 0.0005) and CO (P < 0.005) rose significantly following all three meals. Integrated increments in CO over the postprandial period were greater after 3 MJ compared with the 1 and 2 MJ meals (P < 0.05). SMABF rose significantly following all three meals. The pattern of blood flow response was significantly different between the 1 and 3 MJ meals (interaction effect P < 0.02, ANOVA), with blood flow after the 3 MJ meal being significantly greater than flow after the 1 MJ meal at 15, 60, and 90 min. Similarly, the pattern of response was significantly different after the 2 and 3 MJ meals (interaction effect P < 0.03, ANOVA), with blood flow being significantly greater at 15 and 90 min after the 3 MJ meal. CBF fell significantly in the first 15 min after the 3 MJ meal and then recovered towards baseline values. No other significant changes in CBF were recorded. There are substantial peripheral and central cardiovascular changes after food in man and there appears to be a relationship between meal size and the extent of these changes.

To determine the contribution of tissue protein reserves to lactational performance, multiparous female Sprague-Dawley rats were mated, caged individually and offered a diet high in protein (215 g crude protein (N × 6·25; CP)/kg dry matter (DM);H) ad lib. until day 12 of gestation. Subsequently half the rats continued to receive diet H while the remainder were offered a diet low in protein (65 g CP/kg DM;L) until parturition. This treatment aimed to produce a difference in carcass protein at parturition. On day 1 of lactation females were allocated to either diet H or a low-protein diet (90 g CP/kg DM; L2) offered until day 13 of lactation, giving four lactation treatment groups HH, HL2, LH and LL2. Groups of females were slaughtered on days 2 and 12 of gestation and days 1 and 13 of lactation and carcass and major organs were analysed. Weight gain of standardized litters was used as an indicator of lactational performance. Maternal carcass protein contents at parturition were 43·5 (SE 1·2) and 38·7 (SE 0·8) g (P < 0·01) for diets H and L respectively. During lactation there was little change in carcass protein content of HH rats while LH rats appeared to replenish their depleted reserves. Food intake or lactational performance did not differ between these two groups. HL2 and LL2 rats lost carcass protein with HL2 rats losing more than LL2 rats (P < 0·05). Intake and lactational performance were reduced compared with that on diet H (P < 0.05) but for the first 6 d of lactation were both greater (P < 0·05) for diet HL2 than for diet LL2. All four groups showed a considerable loss of body fat during lactation which was not affected by diet. The ability of HL2 rats to catabolize more protein and consume more food allowed them to sustain a greater lactationai performance. Previous maternal protein depletion had no influence on lactationai performance as long as an adequate supply of dietary protein was provided.

The aim of the study was to determine if there is a difference between ileal and faecal assays for determining amino acid and N digestibilities in adult human subjects. Comparison of true ileal amino acid and N digestibilities was also made between adult human subjects and growing pigs to establish the usefulness of the pig as a model animal. Five subjects with established ileostomies and six subjects with intact large bowels consumed a constant diet consisting of meat, vegetables, fruit, bread and dairy products for 7 d with collection of ileostomy contents or faeces respectively over the last 4 d. The study was repeated using 25 kg body weight ileostomized and intact pigs. Apparent amino acid and N digestibility coefficients were determined. For human subjects the faecal digestibility values were significantly higher (P < 0·05) than the ileal values for Arg, Asp, Gly, Phe, Pro, Ser, Thr and Trp. The faecal digestibility of Met was significantly lower than the ileal value. Determination of DNA, diaminopimelic acid (DAPA) and the digestibilities of pectin, hemicellulose and cellulose in human subjects indicated that some microbial colonization had occurred at the terminal ileum after formation of an ileostomy; however, this was not as extensive as in the large intestine. True ileal amino acid and N digestibilities were calculated after correcting for the endogenous contribution of amino acids at the terminal ileum determined using a protein-free diet. There were no significant differences between adult human subjects and pigs for true ileal dietary amino acid digestibility except for Thr, Phe, Cys and Met. There were no significant differences between adult humans and pigs for the ileal digestibility of dry matter and the faecal digestibility of gross energy.

The action of intravenous infusion of the βagonist cimaterol(2.5 mg/d) on whole-body N retention and protein synthesis in peripheral tissues was examined in growing sheep. Wool growth was determined from skin patch clippings and adjusted to total fibre production. Protein synthesis was measured, using sequential large dose injections of [ l-I3C]valine, leucine and phenylalanine and then [ring-d,]-phenylalanine, on biopsy samples from skin and m. longissirnus dovsi taken before β-agonist administration, at day 3 and day 15 of cimaterol infusion, and 15 d after withdrawal of the drug. Cimaterol increased total N retention by 1.9–2.3 g N/d (P < 0.01) over three successive 5 d periods. In contrast, wool growth was significantly reduced by 0.7 g N/d (P < 0.001) and the proportion of total N retained in wool declined from 0.71 to 0.25 (P < 0.01). The reduction in woo1 growth was accompanied by a decrease in protein fractional synthesis rate (FSR) in skin (11.6 v. 6.3%/d, P < 0.01). Muscle protein FSR, on the other hand, was markedly stimulated during cimaterol infusion (1.45 v. 3.01 %/d, P < 0.001) as was RNA concentration (P < 0.001), RNA:protein (P < 0.001) and protein:DNA (P < 0.05). The estimated increase in total protein synthesis in muscle (+ 24 to 30 g/d) due to cimaterol administration was counterbalanced by reductions for skin (-25 to 27 g/d); this may account for the lack of changes in whole-body protein synthesis following β-agonist administration reported in other studies. Although N retention rapidly returned to control values following withdrawal of the drug, both wool growth and skin protein synthesis remained depressed, while muscle protein FSR declined, but not to pre-treatment values. These results suggest a persistent action of cimaterol, but whether this is a function of residue concentrations or long-term metabolic responses is not known

The objective of the present experiment was to test whether the relationship between feed composition and the efficiency of protein utilization in pigs was different between two very different breeds. Fortyeight entire male pigs, half Large White × Landrace (LW ×) and half Chinese Meishan (CM), were assigned at 13 kg live weight either to an initial slaughter group or to one of six feeding treatments for 6 weeks. The two feeds used were starch, with 12.52 MJ metabolizable energy (ME) and 0 kg digestible crude protein (DCP)/kg, and a high-protein feed, with 11.95 MJ ME and 0.362 kg DCP/kg. In the first week the LW × pigs were given 400 g high-protein feed/d with 0, 100, 200 or 300 g starch/d, or 200 g high-protein feed/d with 400 or 500 g starch/d. The six diets had ME:DCP ratios of between 33 and 119 MJ/kg. The diet compositions were held constant within each of the six treatments but the allowances were increased weekly on time-based linear scales to be 2.25 as great in week six as in week one. The allowances for the CM pigs were 0.75 of those for the LW ×. The calculated efficiency of protein utilization, ep, was found to be directly proportional, up to a maximum value, to the ME:DCP ratio of the diet for both breeds, as found previously for LW × male and female pigs. The overall constant of proportionality was ep = 0.0108 (SE 0.00024) ME:DCP, the value of which did not differ significantly between the two breeds. The maximum observed ep values were 0.710 (SE 0.014) and 0.824 (SE 0.016) for the LW × and CM pigs respectively. It is likely that the lower maximum value for the LW x pigs was an experimental artefact due to increased feed spillage by these pigs on the two highest starch allowances used. In previous experiments the maximum value of ep was found to be 0.813 for LW × pigs, a value similar to that found here for the CM pigs. The results are consistent with the view that the two very different pig breeds have the same net efficiency in using protein and use the same rules for partitioning a scarce resource such as energy.

The ileal digestibility of tryptophan for growing pigs was determined for cottonseed, meat-and-bone and soya-bean meals. Tryptophan in the food and digesta was measured by two analytical procedures (NaOH hydrolysis and colorimetric estimation (method 1) and LiOH hydrolysis and HPLC determination (method 2)). The results were respectively: cottonseed meal 0.46, 0.81; meat-and-bone meal 0.55, 0.65; soya-bean meal 0.74, 0.90. In the first experiment the values for method 1 were shown to be inapplicable to pigs. In a second experiment three tryptophan-deficient diets (005 g ileal digestible tryptophan/MJ digestible energy (DE)) were formulated using values from method 2 for cottonseed meal, meat-and-bone meal plus L-tryptophan and soya-bean meal respectively as the only sources of tryptophan in the diets. This experiment was terminated after 28 d as overall growth performance of the pigs was very low. A third experiment was conducted in a similar manner to Expt 2 except that the diets were formulated to 0.065g ileal digestible tryptophan/MJ DE and growth responses and tryptophan retention were assessed over the 20–45 kg growth phase. Growth rates (g.d) of the pigs given the three diets were significantly different (P < 0.01): cottonseed meal 393, meat-and-bone meal plus L-tryptophan 531, soya-bean meal 437 (SED 39.0). Tryptophan retention (as a proportion of ileal digestible tryptophan intake) was significantly different (P < 0.05): cottonseed meal 0.51, meat-and-bone meal plus L-tryptophan 0.49, soya-bean meal 0.41. These results indicate (1) that the colorimetric technique for assessing tryptophan was inapplicable and (2) that ileal digestible values for tryptophan were not suitable for formulating diets containing heat-processed proteins, possibly due to absorption of some of the tryptophan in a form that was non-utilizable, and/or to underestimation of total tryptophan in the protein concentrates.

To compare the changes in Fe metabolism during the development of vitamin A and Fe deficiencies, rats were given either a control diet with sufficient Fe (35 mg added Fe/kg feed) and retinol (1200 retinol equivalents/kg feed), a diet without added vitamin A or a diet with sufficient vitamin A but only 3.5 mg added Fe/kg feed. During a period of 10 weeks, indicators of vitamin A and Fe status were monitored. Neither vitamin A nor Fe deficiency produced clinical signs. Fe deficiency induced an immediate fall in blood haemoglobin concentration. Vitamin A deficiency produced a mild anaemia as the first change in Fe metabolism, pointing to unpaired erythropoiesis. This effect was followed by a rise in Fe absorption and an increased amount of Fe in the spleen. By the end of the study, blood haemoglobin, packed cell volume, plasma Fe and Fe content in kidney and femur had increased above control levels, while total Fe-binding capacity had decreased. We speculate that the initial anaemia was masked later by haemoconcentration. The decrease in Fe mobilization, shown by lower total Fe-binding capacity, and the increase in Fe absorption may have caused the observed continuous rise in tissue Fe concentration in rats with vitamin A deficiency. In the rats with Fe deficiency, low tissue Fe levels coincided with high Fe absorption and high total Fe-binding capacity. Thus, changes in Fe metabolism with vitamin A deficiency differed from those with Fe deficiency.

Pectin is known as a cholesterol-reducing dietary fibre, and in the present study we addressed the question whether pectin affected the quantity of lipid in droplets in the myocardial cells and of lipid in the liver cells. Male Wistar rats received either a diet containing cholesterol or a standard diet without cholesterol with 0, 50 or 100 g pectin/kg incorporated for 10 d. The fractional volume of lipid droplets in the myocardial cells decreased as a function of pectin dose in both the standard-fed and the cholesterol-fed rats. Serum cholesterol was significantly reduced in both groups after addition of 100 g pectin/kg diet. The cholesterol diet increased the liver cholesterol level, and 100 g pectin/kg diet resulted in a lower concentration of liver cholesterol in the cholesterol-fed animals, but the influence on standard-fed rats was modest. Hydroxymethylglutaryl-CoA reductase (EC 1.1.1.88; HMG-CoA reductase) activity-increased when pectin was given in the standard diet. Liver triacylglycerol level increased after cholesterol and pectin feeding. Mitochondrial fatty acid oxidation and phosphatidate phosphohydrolase (EC 3.1.3.4) activity tended to decrease, whereas the peroxisomal fatty acid oxidation and acyl-CoA oxidase activity were unchanged. Increased hepatic triacylglycerol content by cholesterol and pectin treatment may be due to inhibited mitochondrial fatty acid oxidation along with increased availability of fatty acid for esterification and triacylglycerol synthesis. The presence of pectin in the diets of cholesterol-fed rats resulted in increased hepatic concentration of triacylglycerols and increased mitochondrial fatty acid oxidation. In this case the hepatic accumulation of triacylglycerol may be mediated by a reduced efflux of triacylglycerols from the liver.

We tested the hypothesis that ascorbic acid in the diet of rats lowers the concentration of soluble Cu in the small intestine, causing a decrease in apparent Cu absorption. Male rats were fed on diets adequate in Cu (5 mg Cu/kg) without or with 10 g ascorbic acid/kg. The diet with ascorbic acid was fed for either 6 or 42 d. Ascorbic acid depressed tissue Cu concentrations after a feeding period of 42, but not after 6 d. Dietary ascorbic acid lowered apparent Cu absorption after 6, but not after 42 d. The lowering of tissue Cu concentrations after long-term ascorbic acid feeding may have increased the efficiency of Cu absorption, and thus counteracted the inhibitory effect of ascorbic acid. Dietary ascorbic acid caused a significant decrease in the Cu concentrations in the liquid phase of both the proximal and distal parts of the small intestinal lumen. This effect was due to both a decrease in the amount of Cu in the liquid digesta and an increase in the volume of the liquid phase; only the latter effect for the distal intestine was statistically significant. We conclude that ascorbic acid supplementation lowers Cu absorption by decreasing the concentration of soluble Cu in the small intestine.

Mesenteric bleeding time, mesenteric vascular reactivity, platelet and erythrocyte lipid fatty acid composition were measured at 2–3 weeks, 5–6 weeks and 11–22 weeks in normotensive Wistar rats, fed on high (6·5% energy) or moderate (1·6% energy) intakes of eicosapentaenoic acid (20: 5n−3; EPA) as fish oil, compared with controls fed on a diet devoid of EPA. All diets contained the same level of linoleic acid (4% energy): the moderate- and high-EPA diets also contained 1·1 and 4·4% of the energy as docosahexaenoic acid (22:6n−3) respectively. Moderate, but not high, intakes of EPA increased mesenteric bleeding time. Similar reductions in erythrocyte and platelet arachidonic acid (20: 4n−6) occurred in animals fed on either high or low amounts of EPA, but the proportion of EPA increased dose-dependently. At high intakes of EPA the proportion of oleic acid in platelets and erythrocytes was decreased. Blood pressure platelet counts, mesenteric vessel diameter and mesenteric vascular reactivity to vasopressin were unaffected by treatment. High intakes of fish oil led to a slight fall in packed cell volume. In a second experiment bleeding time and mesenteric vascular reactivity to noradrenaline were increased 2–4 weeks after receiving a moderate intake of EPA and these effects persisted 5–21 d after switching to a control diet. A similar increase in vascular reactivity to noradrenaline was observed in animals given indomethacin (6 mg/kg) but not in those given aspirin (20 mg/kg).

N metabolism was studied in young rats fed on lipid-rich, isonitrogenous, purified liquid diets, a convenient and easy technique for inducing voluntary overfeeding of energy and lipids under controlled nutritional conditions. Overfed rats showed a marked N retention at the expense of a reduced production of urea. The capacities of isolated hepatocytes to synthesize urea and glucose from added precursors were greatly diminished. The activities of the urea cycle enzymes and several enzymes involved in the availability of NH3, for this pathway were concomitantly reduced in overfed animals. Therefore, our results showed an improved N metabolism in overfed rats promoted by the overfeeding of lipids that could be due to an enhanced biosynthetic utilization and a reduced catabolism of amino acids. In addition, the versatile and accurate technique for inducing overfeeding in young rats used in the present study could have many advantages for nutritional studies.

A correlation between dietary lipids and cellular enzyme activities is a problem that has only been partially addressed by nutritionists. Therefore, changes in the fatty acid composition and the activities of some key metabolic enzymes (ubiquinol-2-cytochrome c reductase (EC 1.10.2.2), cytochrome oxidase (EC 1.9.3.1) and ATPase (EC 3.6.1.3)) in the mitochondria of liver, heart and brain of rats fed on diets differing extensively in their polyunsaturated fatty acid compositions have been investigated. The results showed that fatty acid compositional changes brought about by the dietary differences were associated with extensive changes in the activities of these key enzymes in the mitochondria. The extent of the influence differed considerably with the period over which the diets were fed. The role of dietary lipids to effect changes through the preservation of membrane structural integrity is discussed.

Guanidinated proteins when fed to non-ruminants provide values for both endogenous amino acid losses and amino acid digestibilities, provided that the homoarginine residues in the treated protein are randomly distributed. Earlier studies have established that guanidination has only minor effects on the structure of the protein and, in particular, on its susceptibility to proteolysis. Furthermore, we have confirmed that homoarginine behaves as a typical amino acid in the small intestine. Lysine residues in casein and soya-bean protein, and in the proteins of cotton-seed meal, meat meal, soya-bean meal, maize, sorghum and wheat were converted to homoarginine by guanidination, the extent of conversion ranging from 37–68%. Sequential proteolysis in vitro of these guanidinated materials showed that the ratios of homoarginine to other amino acids remained unchanged for casein and soya-bean protein, indicating random distribution of homoarginine residues, but not for all the amino acids in meals and cereals. The use of guanidinated casein as the sole protein source in diets fed to broiler chickens allowed measurement of endogenous losses of amino acids under normal feeding conditions and calculation of true digestibilities of dietary amino acids at the ileum. Endogenous amino acid losses measured by the use of guanidinated casein (15.3 g/kg dry matter (DM) intake) were significantly higher (P < 0.001) than values obtained by feeding a N-free diet (5.4 g/kg DM intake), or by regression analysis to zero N intake (72 g/kg DM intake)

The effects of rye bran, oat bran and soya-bean fibre on serum lipids, bile composition and gallstone formation were studied in male Syrian golden hamsters (Mesocricetus auratus). The control groups received fibre-free stone-provoking (O1 diet) or non-stone-provoking (O2 diet) diets. The serum cholesterol levels were lower for all groups fed on the diets supplemented with the dietary fibre sources compared with the control groups. The total content of bile acids in bile was higher in groups given ryebran diets compared with the corresponding controls. The proportion of cholic acid was higher and that of chenodeoxycholic and lithocholic acid lower in the groups given rye-bran-, oat-bran- or soya-bean-fibre-supplemented diets, compared with the corresponding controls. The secondary: primary bile acid ratio was lower in the group given the rye-bran-supplemented O1 diet. The lithocholic:deoxycholic acid ratio was lower in the groups given rye-bran-, oat-bran- or soya-bean-fibre-supplemented diets than in the corresponding controls. A lower frequency of gallstones was observed only for the group receiving the rye-bran-supplemented O1 diet while the lithogenic index was lower in the groups given the rye-bran-supplemented O2 diet. A decreased epithelial volume density of the gall-bladder and an increased smooth muscular volume density were observed in animals given oat-bran- and rye-bran-supplemented O1 diets, whereas for the soya-bean-fibre-supplemented O1 diet, only the smooth muscular volume density was increased.

The present study examines the effects of dietary saturated (hydrogenated coconut oil) and polyunsaturated (salmon oil) fats on the composition and metabolism of lipoproteins in growing rats fed on protein-deficient diets. Four groups of rats were fed on the following diets for 28 d: 200 g casein+50 g coconut oil (COC)/kg, 20 g casein+50 g coconut oil (COd)/kg, 200 g casein + 50 g salmon oil (SAC)/kg, 20 g casein+50 g salmon oil (SAd)/kg. Both protein-deficient groups exhibited low concentrations of protein and triacylglycerol (in serum, very-low-density lipoprotein (VLDL), low-density lipoprotein-high-density lipoprotein, (LDL-HDL1) and HDL2-3), of cholesterol (in LDL-HDL1) and of phospholipids (in VLDL). Furthermore, serum and VLDL cholesterol concentrations were also reduced in the SAd group. Compared with rats given 200 g casein/kg diets, those fed on low-protein diets presented lower linoleic and arachidonic acid levels, in serum phospholipids and a dramatic decrease in the polyunsaturated: saturated fatty acid value. Relative amounts of linoleic and arachidonic acids in phospholipids of VLDL and HDL2-3 were also lowered in the Cod group but not in the SAd group. However, proportions of 22:5n-6 and 22:6n-3 in VLDL and HDL2-3 phospholipid fractions were enhanced in the Cod and SAd groups respectively. The most affected apolipoproteins (apo) were apo B100 and apo B48 in rats fed on protein-deficient diets, apo A1 and apo E in the Cod group, and apo AIV, in the SAd group. Compared with rats fed hydrogenated coconut oil diets, those fed salmon oil diets had enhanced LDL-HDL1 and HDL2-3 but lower VLDL total apolipoproteins (mainly due to a fall in apo B100, and apo B48). Arachidonic and eicosapentaenoic acids, which are impaired by protein deficiency, are the precursors of prostaglandins, thromboxanes and leukotrienes which are implicated in a number of regulatory processes. Our results demonstrate that protein malnutrition is associated with impaired metabolism of arachidonic and eicosapentaenoic acids. Protein malnutrition and essential fatty acid (EFA) deficiency are characterized by many common clinical features and the Link between the two may be an impaired production of eicosanoids, since arachidonic and eicosapentaenoic acids are the precursors of these important metabolic regulators. Because of the apparent involvement of EFA deficiency in the aetiology of protein malnutrition, it may he prudent to include adequate amounts of EFA in diets of infants suffering from kwashiorkor.

The effect of heated sunflower oil consumption on α-tocopherol status, fatty acid composition and oxidative stability of chicken tissues was investigated. Chicks were fed on diets containing (g/kg): fresh sunflower oil (FSO) 40, heated sunflower oil (HSO) 40 or heated sunflower oil (40) supplemented with α-tocopheryl acetate (HSE) to a similar α-tocopherol concentration as the FSO diet. Concentrations of α-tocopherol in tissues of chicks fed on HSO and HSE were significantly lower than those of chicks fed on FSO. Significant correlations were observed between plasma α-tocopherol concentration and the α-tocopherol concentrations of other tissues (r < 0·67, P < 0·005) and between log plasma α-tocopherol and plasma thiobarbituric acid-reacting substances (TBARS) concentrations (r – 0·851, P < 0·001). The concentrations of TEARS in tissues of chicks fed on the various diets were generally very similar before stimulation of peroxidation with Fe–ascorbate. Susceptibility of tissues to Fe–ascorbate-induced lipid peroxidation was increased by feeding HSO. Supplementation with α-tocopheryl acetate reduced susceptibility tc lipid oxidation to varying degrees, depending on the tissue. The results suggest that chronic ingesrion of oxidized lipids may compromise free-radical-scavenging activity in vivo by depleting α-tocopherol in the gastrointestinal tract, or possibly in plasma and other tissues.

Two experiments were conducted to determine the utilization of ileal digestible isoleucine by growing pigs. In the first, the apparent ileal digestibility of amino acids in cottonseed meal, lupin-seed meal and soya-bean meal was determined in pigs fitted with‘T‘-shaped cannulas. In the second, three isoleucine-deficient diets were formulated to 0.23 g ileal digestible isoleucine/MJ digestible energy (DE) with the three protein concentrates contributing the only source of isoleucine in sucrose-based diets. An additional three diets were formulated with supplements of isoleucine to confirm that isoleucine was limiting in the first three diets. The growth performance and retention of isoleucine by pigs given the six diets over the 20–45 kg growth phase were then determined. The apparent ileal digestibility of isoleucine in the three protein concentrates (proportion of total) was: cottonseed meal 0.68, lupin-seed meal 0.86, soya-bean meal 0.86. There were no significant differences (P > 0.05) in growth rates (g/d) and crude protein deposition rates (g/d) of the pigs given the three diets formulated to 0.23 g ileal digestible isoleucine/MJ DE: cottonseed meal 590, 84; lupin-seed meal 613, 87; soya-bean meal 594, 91 (SEM 13.0, 2.9) respectively. The response of pigs to the addition of isoleucine confirmed that isoleucine was limiting in these diets. The proportion of ileal digestible isoleucine retained by pigs given the cottonseed meal (0.65) was slightly lower than that retained by pigs given soya-bean meal (0.73; P < 0.05). These results indicate that values for the ileal digestibility of isoleucine in protein concentrates more closely reflect the proportion of isoleucine that can be utilized by the pig than occurs for other amino acids such as lysine, threonine and methionine.

Whether the association with gut microflora modifies the energy metabolism of chickens was investigated by varying the metabolizable energy consumption level from zero to above the maintenance requirement in the germ-free and conventional states. Single comb White Leghorn chicks were either fasted for 3 d (Expt 1), or fed for 6 d at a fixed daily meal intake of 2, 5 or 8 g/d (Expt 2), or 5, 10 or 15 g/d (Expt 3). Changes in carcass energy deposition and heat production indicated that when no dietary energy was available the presence of the gut microflora could benefit the birds by reducing energy losses, whereas when dietary energy was supplied the efficiency of energy utilization was reduced by the presence of the gut microflora. It was concluded, therefore, that the heavy burden of the gut microflora modifies energy metabolism by exerting a buffering or a counter-productive action on the energy utilization of the chicken.