The effects of amount and type of dietary fish proteins on plasma and liver cholesterol concentrations were evaluated in female rats. The isonitrogenous diets used contained 10 g cholesterol/kg and were carefully balanced for residual fat, cholesterol, Ca, Mg and P in the protein preparations. Cod meal, soya-bean protein or casein was incorporated into the diets as the only source of dietary protein a t three levels: either 24,48 or 72 g N/kg diet. Extra protein was added to the diet at the expense of the glucose component. In a second experiment soya-bean protein, casein, cod meal, whiting meal or plaice meal was added to the diet at a level of 24 g N/kg. When compared with casein, cod meal and soya-bean protein decreased plasma and liver cholesterol concentrations. A further cholesterol-lowering effect was achieved by increasing the proportion of either soya-bean protein or cod meal in the diet. Substitution of casein for glucose did not influence plasma and liver cholesterol concentrations. Plaice meal in the diet produced lower group mean plasma cholesterol concentrations than did whiting meal. In rats fed on the diet containing plaice meal, liver cholesterol concentrations were significantly lower than those in their counterparts fed on either cod meal or whiting meal. The present study demonstrates that different fish proteins in the diet have different effects on cholesterol metabolism and that the cholesterol-influencing properties of cod meal can be enhanced by the incorporation of higher proportions of this protein in the diet.

In a study with twelve pigs of 60–70 kg live weight provided with a re-entrant cannula at the end of the ileum, and twelve intact, non-cannulated pigs, the fate of dietary doses of 100 and 200 g isomalt/kg during gastrointestinal passage was examined. From sugar analyses in ileal chyme it was calculated that 0.43 and 0.30 of the isomalt consumed was digested in the small intestine with the 100 and 200 g/kg doses of isomalt respectively. From findings on ileal energy digestibility it was calculated that, because of a secondary effect of isomalt on the digestion of the basal diet, isomalt digestibility in the small intestine was distinctly lower. In faeces no sugars were found, so faecal digestibility of isomalt was 1.00 for both doses. The bacterial fermentation in the large intestine of the isomalt not digested in the small intestine caused an increase in the faecal excretion of nitrogen and energy. This increased faecal excretion was hardly (nitrogen) or not (energy) compensated by a decreased urinary excretion.

Eleven Holstein bull calves 35 d of age were assigned to one of three treatment groups: (1) W72, warm environment (20°), 72 g feed/kg body weight (BW)0.75 per d, (2) C72, cold environment (−5°), 72 g feed/kg BW0·75 per d, or (3) C90, cold environment (−5°), 90 g feed/kg BW0·75 per d. Fractional synthesis rates (FSR) of protein in the rumen wall, rumen papillae, omasum, duodenum, kidney, liver,heart, longissimus dorsi, biceps femoris and skin were determined following a continuous infusion of[3H]phenylalanine. Phenylalanine flux was elevated in both groups of cold-adapted calves. FSR of protein in the two muscles and skin were reduced along with N retention in the calves in the C72 group compared with the other two groups. Muscle protein degradation, estimated from urinary Nτ-methylhistidine excretion, tended to be elevated in both groups of cold-adapted calves. Reduced protein synthesis and increased protein degradation in the C72 group contributed to reduced muscle protein gain. It appears that when feed intake is limited in cold-adapted animals, muscle and skin have a lower priority for nutrients than other organs and tissues, resulting in reduced protein synthesis, it seems unlikely that thermogenesis due to enhanced protein synthesis contributed to the increased heat production in the cold.

In a study with ten pigs of 60–70 kg live weight, provided with a re-entrant cannula at the end of the ileum, and sixteen intact, non-cannulated pigs, the digestion and absorption of a dietary dose of 100 g isomalt/kg, and isomalt given between the meals as a ‘sweet’on the basis of 50 and 100 g/kg feed consumption, were examined. In all three isomalt treatments slightly less than 0.40 of the isomalt consumed was digested in the small intestine when the calculations were based on ileal sugar passage. However, when basing the calculations on energy contents of ileal chyme, only approximately 0.10 was digested in the small intestine. The bacterial fermentation of the isomalt flowing into the large intestine was indicated by a decreased faecal energy digestibility and a slight reduction in faecal dry matter and nitrogen digestibility. The retention of the minerals sodium, potassium, magnesium, calcium and phosphorus was not influenced to any measurable extent when isomalt was fed.

To study the effects of medium-chain triacylglycerols (MCT) on maternal lipid metabolism and pup growth, MCT (200 g/kg) were incorporated into a commercial chow diet and fed to lactating rats for 8–10 d. The results were compared with similar diets containing sunflower oil (polyunsaturated fatty acids; PUFA), tristearin (saturated fatty acid) or triolein (monounsaturated fatty acid). There was decreased food and energy intake with the MCT diet and this was accompanied by decreased (35%) pup growth. All the high-fat diets inhibited lipogenesis in vivo in the lactating mammary gland, the order of effectiveness being PUFA > triolein > tristearin > MCT. Only the MCT diet increased the rate of hepatic lipogenesis (180%). Experiments feeding an MCT meal containing [l-14C]octanoate indicated that very little (3–4%) of the C was present in mammary gland lipid, unlike the findings with [l-14C]triolein meal (40%). The major portion (65%) of the absorbed [l-I4C]octanoate was oxidized to 14CO2. There was no evidence for adaptation of the mammary gland to increased dietary lipid uptake on the triolein or MCT diets. It is concluded that the decreased pup growth on the MCT diet is due in part to the decreased energy intake and to the inability of dietary medium-chain fatty acids to provide substrates for milk lipid synthesis.

The role of the soluble non-starch polysaccharide pectin in the prevention of oxidative damage induced by peroxy, superoxide and hydroxyl radicals to the rat jejunal mucosa was studied. The oxidative stress was introduced to the rat jejunal mucosa by means of a closed-loop perfusion system and was characterized biochemically by monitoring the enterocyte activity of the enzyme lactate dehydrogenase (EC 1·1·1·27) and the K+ level. Aqueous solutions of pectin were perfused into the rat jejunum before the oxidative stress inducers. The possible protection effect was evaluated by comparing the mucosal integrity (as measured by biochemical variables) to the values obtained after perfusion with the oxidative stress inducers only. We found that: (a) mucosal damage was detected following the perfusion of peroxy and hydroxyl radicals in the rat jejunum, but not following perfusion of the superoxide radical; (b) a significant reduction in the mucosal damage was noted when pectin was perfused before the perfusion with the peroxy radical induction; (c) full protection against the mucosal damage induced by hydroxyl radicals was achieved when pectin was perfused before the damage induction.

To obtain quantitative information on the digestibility of the non-starch polysaccharides (NSP) fraction of white and wholemeal breads, rats were fed on diets in which freeze-dried bread (white, wholemeal or mixtures of the two) provided all the complex carbohydrates. In a second experiment the possibility that dietary fat concentration might influence NSP digestibility was tested by feeding diets containing 30 or 170 g maize oil/kg and either white or wholemeal bread. Multiple linear regression analysis provided little evidence of associative effects of dietary components on NSP digestibility and in the two experiments digestibilities of NSP for white and wholemeal breads were 0·77–0·82 and 0·47–0·52 respectively. Xylose- and arabinose-containing polymers were better digested than was cellulose for both breads. Replacing white by wholemeal bread markedly increased the molar proportion of butyrate in caecal volatile fatty acids at the expense of acetate. This was associated with greater flows of organic matter to the large bowel (LB) and a reduction in caecal transit time (Expt 2). There was little detectable ettect of dietary maize oil concentration on NSP digestibility or on LB fermentation. All breads contained some starch resistant to pancreatic α-amylase (EC 3.2.1.1) without previous treatment with dimethyl sulphoxide. The digestibility of this starch fraction was not significantly different from 1·0 for all diets except that containing wholemeal bread and the higher maize oil concentration where the apparent digestibility was 0·89.

Guinea-pigs were undernourished from birth by first, cross-fostering in groups of six (in pairs for control animals) and then by feeding a diet of 60% of ad lib. intake from 2 to 6 weeks. The changing characteristics of muscle fibre types in the biceps brachii and soleus muscles were monitored by histochemistry. Undernutrition appeared to delay maturation of muscle fibres. Fibre cross-sectioned area was reduced in all fibres of the 60% of ad lib. intake group. Fibres of the biceps brachii were more affected than those of the soleus. Fibre area vulnerability was partly associated with a high relative growth rate in biceps brachii at this time. Total protein content in the semitendinosus muscle was depressed in the undernourished group compared with the control group. DNA concentrations were initially higher in the control group but decreased in both groups to similar levels by 6 weeks. RNA concentration increased up to 5 weeks in the control group and then decreased, but decreased after 2 weeks in the undernourished group.

The effect of dietary fats on gastrin in the pyloric antrum and plasma of Wistar rats was examined. Two different age-groups of rats were fed on three different diets in which fat was in the form of menhadenoil (MO), hydrogenated coconut oil (CO) and safflower oil (SO) respectively. Control groups were fed on normal laboratory diet. Each diet was isoenergetic and no group showed significant differences in either food intake or weight gain during the experiment. Weaner rats fed on the MO diet exhibited significant reductions in both antral (P = 0.047) and plasma (P = 0.002) gastrin concentrations when compared with age-matched controls. Likewise, adult rats fed on the MO diet exhibited significant reductions in both antral (P = 0.008) and plasma (P = 0.002) gastrin concentrations. In addition, adult rats fed on the CO diet exhibited significant reductions in both antral (P = 0.047) and plasma gastrin(P = 0.002) concentrations. Rats from both age-groups fed on the SO diet exhibited no significant differences in gastrin concentrations when compared with their respective control groups. These findings indicate that the composition of dietary fat can have profound effects on both tissue and plasma concentrations of gastrin in rats.

The effects of folate sufficiency and deficiency in three pathways of folate metabolism were studied in 2- and 3-week-old broiler chicks. Erythrocyte phosphoribosylpyrophosphate concentrations and dihydro- folate reductase (EC 1.5.1.3) activity were significantly elevated in folate deficiency. Percentage incorporation of deoxyuridine into bone marrow DNA was reduced in folate deficiency. There was a trend towards reduced liver dihydrofolate reductase activity in deficient chicks. These studies identify further biochemical criteria that can be used to assess folate status of chicks.

The digestion of non-starch polysaccharides (NSP) and of resistant starch (RS) by rats fed on wholemeal-bread-based diets containing 0-450 g cooked, freeze-dried haricot beans (Phaseolus vulgavis)/kg diet was measured over the final 14 d of a 21 d feeding experiment. The bread and beans provided all the dietary polysaccharide. RS could not be detected consistently in faeces and it was assumed that this fraction was entirely fermented in the large bowel (LB). NSP digestibilities were 0.56 and 0.86 for wholemeal bread and beans respectively with no evidence that the dietary presence of beans affected digestibility of bread NSP. Bean non-cellulosic polysaccharides were highly digestible with values of 0.98, 0.88 and 0.99 for arabinose, xylose and uronic acids components respectively. There were large increases in organic matter flow to the LB when beans were fed which was associated with marked caecal hypertrophy and alterations in caecal volatile fatty acids (VFA) pattern. Calculated VFA absorption from the LB was 5-fold higher with the highest level of beans and this was reflected in higher concentrations of VFA in portal and heart blood.

Three experiments were carried out to investigate the effects of supplemental dietary 1·25-dihydroxycholecalciferol (1·25(OH)2cholecalciferol) and a low dietary Ca:P ratio on the occurrence of tibial dyschondroplasia (TD) in 3-week-old broilers. Histopathology was used to diagnose TD. In the first experiment, feeding a diet containing 7·5 g Ca and 7·6 g P/kg gave a higher incidence of TD than a control diet containing normal amounts of Ca and P (12 and 6 g/kg respectively). Increasing the dietary supplement of cholecalciferol in the imbalanced diet prevented rickets but did not decrease the incidence of TD. In the second experiment, supplementing the imbalanced diet with 10 μg 1·25(OH)2cholecalciferol/kg prevented TD completely but also gave a slight growth depression. In the third experiment the imbalanced diet was supplemented with 0, 2·5, 5 or 10 μg 1·25(OH)2 cholecalciferol/kg. The supplement of 2·5 μg/kg depressed and the higher supplements prevented the occurrence of TD, this time without a growth depression. Feeding the 10 μg/kg supplement for the first week only did not prevent TD. Plasma total Ca, inorganic P and alkaline phosphatase (EC 3·1·3·1) were unaffected by diet but 1·25(OH)2cholecalciferol was higher on the imbalanced than on the control diet. Supplementation of the imbalanced diet with 1·25(OH)2cholecalciferol did not increase plasma levels. It is concluded that 1·25(OH)2cholecalciferol is exerting a powerful biological effect in this model of TD, but the mechanism is unclear.

In the present study the effect of replacement of dietary fat by palm oil in the normal Western diet on the in vitro release of the inflammatory cytokines tumour necrosis factor (TNF), interleukin (IL)-6 andIL-8 was examined. A maximal replacement of 700 g/kg dietary fat was achieved for thirty-eight male volunteers who consumed either a palm-oil diet or a control diet in a double-blind, cross-over study with6-week experimental periods, and 3-week run-in and wash-out periods. At the end of both experimental periods, whole blood was stimulated in vitro with 0.02 (sub-optimal), or 10 ng lipopolysaccharide(LPS)/ml (maximal), whereafter TNF, IL-6, and IL-8 concentrations in the culture supernatant fraction were measured using specific enzyme-linked immunosorbent assays (ELISA). Mean cytokine production with sub-optimal, or maximal LPS stimulation of peripheral whole blood was similar for both the palm oil, and the control group. The relative TNF response, however, was reduced by replacement of dietary fat with palm oil. Separate analysis of the data from the first and second experimental periods strongly suggested that the residual effect of the palm-oil diet on the relative TNF response was longer than 9weeks. Cytokine homeostasis determines the course of the inflammatory response and the progression of atherosclerosis. The effect of palm-oil consumption on the proneness of the peripheral blood cells to produce TNF may, therefore, alter the prevalence of these common diseases.

In four experiments growing pigs were given a cereal-based diet alone or supplemented with unmolassed sugar-beet pulp (SBP), used as a model substrate for fermentation. The rates of production of methane and gaseous hydrogen were measured and, together with the molar proportions of volatile fatty acids (VFA) in the digesta, used in stoichiometric calculations of fermentation. The resulting estimates were only one-sixth of the observed extent of digestion of SBP. Bacteriostatic levels of antibiotics reduced fermentation by more than half, as judged from the digestion of non-starch polysaccharides: allowing for the incomplete suppression of fermentation it was estimated that the production of methane and VFA could account completely for the digested SBP. The potential contribution of various routes of hydrogen disposal to the error of the stoichiometric calculations is discussed.

The metabolism of erythritol was assessed in six normal volunteers by measuring the amount of 13CO2 excretion and H2 excretion in breath, and erythritol in urine after intake of 25 g 13C-labelled erythritol. The results were compared with the same variables obtained after intake of 25 g 13C-labelled glucose and13C-labelled lactitol. In addition, the H2 production by faecal flora supplemented with small amounts of erythritol, glucose and lactitol was measured in vitro, as an index of bacterial metabolism of non-absorbed substrate. In contrast to the results obtained after intake of glucose and lactitol, no increase in breath 13CO2 and H2 was observed after intake of erythritol, and erythritol was nearly completely recovered in urine. The in vitro experiments showed that no H2 was formed by faecal flora from erythritol as compared with glucose and lactitol. It is concluded that erythritol is a substrate that is readily absorbed, and undergoes no metabolism by the host. If part of it escapes absorption, it is not metabolized by faecal flora.

The effect of Ascaris lumbricoides infection on retinol absorption was investigated in young children from a slum area of Dhaka City, Bangladesh. Twenty-four children aged 4–10 years were screened and in every case eggs of either Ascaris, Trichuris or hookworm were isolated from the stool. The average serum retinol was 0.91 (sd 0.35) μmol/l and sixteen children had levels below 1.05 μmol/l. This compared with a serum retinol concentration of 1.70 (sd 0.52) μmol/l in five reference children from a more privileged social background. An oral dose of retinol (41.8 μmol) was given, to ten children in whom the concentration of Ascaris eggs in the stool varied. Less than 1% of the supplement could be recovered in the stools collected over the following 48 h. Ascaris worms were isolated from the stool and assayed for retinol content. In no case was retinol detected in the worms. These findings do not support the contention that infection with Ascaris predisposes to malabsorption of vitamin A.

Rats were weaned onto high (HCa, 14.6 g/kg)- or low (LCa, 3.88 g/kg)-Ca diets for 12 d and the efficiency of absorption of Ca measured from 20 mg Ca (as CaCl2, labelled with 47Ca) by means of wholebody counting. The LCa group absorbed 74 % of the test dose and the HCa group 60 % of the test dose (P < 0.001). All animals were then given the LCa diet for 6 weeks and the absorption test repeated. This time there was no difference in efficiency of absorption (HCa 54%, LCa 57%). The femur dry weight was significantly lower in the group initially fed on the LCa diet, but the Ca concentration was similar to that of the HCa group. The results do not lend support to the suggestion that early dietary exposure to Ca manifests itself as a difference in Ca metabolism in later life. They do, however, highlight the importance of adequate Ca intake during critical periods of growth.

The ability to hydrolyse and absorb pteroylpolyglutamates (PteGlun) included in a standard meal in mothers who had given birth to an infant with a neural tube defect was tested by comparing them with mothers who had not had any infants with this defect. When compared with control mothers working in the research unit in which the study was performed, case mothers had significantly lower baseline serum and erythrocyte folate levels, and smaller increases in serum folate following the meal containing PteGlun. However, all estimates of folate were similar when case mothers were compared with a group of mothers who were friends of the case mothers. The results show that the higher the baseline levels of serum and erythrocyte folate the greater the increase in serum folate after the test meal. Fitting a model for the serum folate response curve resulted in coefficients which differed significantly between case mothers and all control mothers. We conclude that intestinal hydrolysis of PteGlun taken orally is not impaired in mothers who have had infants with neural tube defects when compared with control mothers with similar baseline folate levels, although the curves describing the response to the meal for the two groups do differ significantly. Further investigation is required to determine the mechanism underlying this difference.

Uniformly 14C-labelled primary cell walls (14C-PCW) were purified from suspension-cultured cells of spinach (Spinacia oleracea L.) grown in a medium containing D-[U-14C]glucose. The approximate polymer composition of the 14C-PCW preparation (% total 14C) was homogalacturonan 30,rhamnogalacturonan 23, xyloglucan 10, other hemicelluloses 3, cellulose 21, lignin 0,14C-labelled protein < 3 and [14C]starch < 2. The degree of methyl esterification of the pectic polysaccharides was about 25%. The 14C-PCW contained about 4% O-acetyl and 3% non-volatile ester-linked residues. When tracer levels of these 14C-PCW were fed to rats, only about 18% of the 14C appeared in the faeces;negligible levels of 14C (0.07%) remained in the gut contents 4 d after feeding. Some 14C was present in the carcass. The results show that U-14C-labelled primary cell walls can be purified and radiochemically analysed by the methods developed here, and that primary cell walls are extensively fermented by the gut microflora of the rat.

The inhibiting effect of Ca on non-haem-Fe absorption is well established. Presentstudies showed that Ca inhibited haem-Fe absorption to the same extent when the same amount of Ca (165 mg Ca as CaCl2) was added to a meal. Attempts were made to examine the mechanism for this inhibition in the present studies. Meat is the only known dietary factor influencing haem-Fe absorption. The present studies were designed to examine whether Ca interfered with the enhancing effect of meat on haem-Fe absorption. We found that the inhibition was the same whether biosynthetically radio-Fe-labelled haemoglobin wasgiven in meals with or without meat. The haem-Fe absorption ratio with: without added Cawas 0.59 (SE 0.07) when Ca was added to a hamburger meal, and 0.052 (se 0.03) when added to a wheat roll. These values were not significantly different (t 0.95; P = 0.35). The inhibition of haem-Fe absorption by Ca is, thus, a direct effect on theabsorption of haem-Fe and not an indirect counteracting effect of the well-known enhancing effect of meat on haem-Fe absorption. Control studies were conducted to ensure that haem-Fe had not been degraded to non-haem-Fe during preparation of the foods. Since Ca inhibits the absorption of haem- and non-haem-Fe to the same extent, the present results strongly suggest that Ca interferes with the transport of Fe through the mucosal cell, andata late stage, is common for haemand non-haem-Fe transport. The observations that Ca strongly interferes with the absorption of both haem- and non-haem-Fe have important nutritionalimplications.