Epidemiological evidence has suggested that the declining prevalence of duodenal ulcer disease may be attributable to rising consumption of polyunsaturated fatty acids, a hypothesis supported by in vitro evidence of toxicity of such substances to Helicobacter pylori. The objective of the present study was to establish whether this association is causal. Forty patients with proven infection with H. pylori and endoscopic evidence of past or present duodenal ulcer disease were randomized to receive either polyunsaturated fatty acids (PUFA group), in the form of capsules and margarine, or a placebo (control). Both groups received concurrent H2 antagonist therapy. Efficacy of therapy was determined endoscopically by assessment of ulcer healing while H. pylori status was determined by antral biopsy, urease (EC 3.5.1.5) culture and histological assessment of the severity of H. pylori infection. Antral levels of prostaglandin E2 (PGE2) and leukotriene B4 (LTB4) were quantified. Compliance was monitored. Before treatment, both groups were comparable for severity of H. pylori infection, smoking status and levels of LTB4 and PGE2. Despite a significant difference in consumption of linoleic acid (19.9 (se) 1.6) g for PUFA group ν. 6.7 (se 0.8) g for controls (P < 0.01) and linolenic acid (2.6 (se) 0.2) g ν. 0.6 (se 0.03) g (P < 0.01) there was no significant change in either the severity of H. pylori infection or prostaglandin levels in either group at 6 weeks. Consumption of a considerable amount of PUFA does not inhibit the colonization of the stomach by H. pylori nor does this alter the inflammatory changes characteristic of H. pylori gastritis. We conclude that the association between duodenal ulceration and a low level of dietary PUFA is likely to be spurious, probably reflecting the effect of confounding factors such as affluence, social class or smoking.

Pregnancy in insulin-dependent diabetes mellitus is associated with a greater incidence of fetal abnormality. Animal studies suggest that increased free-radical production and antioxidant depletion may contribute to this risk. The aim of the present study was, therefore, to assess nutritional antioxidant status and lipid peroxidation in diabetic mothers in comparison with a control group. A 7 d dietary history and a food-frequency questionnaire were performed and venous blood collected for biochemical analyses from thirty-eight diabetic mothers and matched control subjects before 12 weeks gestation. Protein intake was significantly greater in diabetic patients (81.4 (se 14.8) ν. 72.7 (se 15.8) g/d, P = 0.015), while total sugar intake was less (79.5 (se 13.2) ν. 104.8 (se 28.8) g/d, P < 0.001). There were no significant differences in the intake of the major antioxidant vitamins (retinol, vitamin C or vitamin E) or β-carotene. However, intakes of a number of other micronutrients (including Se, Zn, Mg, Mn, riboflavin, thiamin, niacin and folate) were greater in diabetic patients. Among the nutritional chain-breaking antioxidants, serum levels of α-tocopherol (21.6 (se 5.7) ν. 17.3 (se 4.7) μmol/1, P = 0.0013), β-carotene (0.27 (se 0.18) ν. 0.14 (se 0.11) μmol/1, P = 0.003) and lycopene (0.23 (se 0.17) ν. 0.16 (se 0.13) μmol/1, P = 0.03) were greater in diabetic patients. There was no evidence of greater lipid peroxidation in diabetic patients, and total antioxidant capacity was similar in the two groups. Overall, these results indicate that nutritional antioxidant status is better in this group of diabetic mothers than in control pregnant non-diabetic subjects attending the same maternity hospital.

The ileal digestibilities of maize starch and native pea starch do not differ. However maize starch is digested faster than pea starch and the ileal amino acid digestibility of a diet containing pea starch is lower. In the present study, the net portal fluxes of glucose, lactate, volatile fatty acids (VFA) and amino acids were measured for diets including 650 g maize starch or pea starch/kg. The diets were fed at a level 870 kJ digestible energy/kg0.75 twice daily (06.00 and 18.00 hours) to four female pigs in a crossover design. Portal vein blood flow did not differ between maize and pea starches (1620 and 1484 ml/min respectively; sed 100; P = 0.23). For maize starch portal glucose flux was significantly higher during the first 6 h after feeding, was not different 8 h after feeding and was significantly lower thereafter. Net portal glucose flux was higher for maize starch than for pea starch (1759 and 1265 mmol/12 h respectively; sed 182; P = 0.054). Net portal lactate flux was not significantly different between maize and pea starches (36.5 and 67.2 mmol/12 h respectively; sed 24.1; P = 0.27) and net portal VFA flux was lower for maize starch than for pea starch (169 and 218 mmol/12 h respectively; SED 18; P = 0.054). Net portal fluxes of valine, isoleucine, phenylalanine, tryptophan, arginine, serine, cystine, tyrosine, lysine, histidine and the sum of essential amino acids tended to be or were higher (P < 0.1 or P<0.05) and net portal flux of aspartic acid tended to be lower for pea starch (P<0.1). It can be concluded that, although ileal digestibility of both starches is equal, the rate of appearance of glucose in the portal vein was higher for maize starch, influencing the net portal flux of amino acids.

We suggested that food preference depends on the interplay between flavour and post-ingestive effects, and we predicted that protein-restricted lambs would acquire preferences for foods paired with supplemental sources of N, including urea (Expts 1 and 2), casein (Expt 3), and gluten (Expt 4). In each experiment, twenty lambs, in two groups of ten, were conditioned as follows: on odd-numbered days, lambs in group 1 received wheat straw (Expts 1, 3, and 4) or ground barley (Expt 2) flavoured with a distinctive flavour, and lambs in group 2 received the same food but with a different flavour. On even-numbered days, flavours were switched and lambs received capsules containing different amounts of urea (ranging from 0.12 to 0.92 g N/d), casein (ranging from 0.23 to 0.69 g N/d), or gluten (ranging from 0.23 to 0.69 g N/d). After conditioning periods of 8 d, lambs were given a two-choice test to determine preference for flavours paired with N. In Expts 1 and 2, lambs preferred the flavours conditioned with urea at lower doses (0.12 g N/d in Expt 1. 0.23 and 0.46 g N/d in Expt 2), but they avoided the flavour associated with urea at the highest dose (0.23 g N/d in Expt 1 and 0.92 g N/d in Expt 2). In Expts 3 and 4, lambs avoided the flavours associated with the lowest doses of casein or gluten (0.23 g N/d), but they preferred the flavours paired with casein or gluten at higher doses (0.46 and 0.69 g N/d). After conditioning, N administrations were suspended and lambs in Expts 3 and 4 were offered a choice of the two flavours at weekly intervals for 2 weeks (extinction); preferences persisted during extinction. Collectively, these results suggest that the post-ingestive effects of N in different forms and concentrations influenced the development of food preferences by lambs.

Mechanistic rumen models of Baldwin (1995), Danfæer (1990) and Dijkstra et al. (1992) were compared on identical inputs that were derived from trials with lactating dairy cows fed on grass herbage. Consistent differences were detected between models and between predicted and observed outputs. None of the models seemed to predict all nutrient flows best. The models particularly differed in the representation of microbial metabolism: degradation of insoluble substrate, fermentation of substrate into volatile fatty acids, and incorporation of substrate into microbial matter. Differences amongst models in the prediction of these processes compensated for each other and consequently all models predicted the duodenal flow of non-NH3 N, microbial N and organic matter reasonably well. Large differences remained in the prediction of individual nutrient flows, however, and it was stressed that in order to enhance prediction of the profile of nutrient flows, the mechanisms of microbial metabolism need to be tested on their ability to describe the intraruminal transactions. However, this requires more-detailed information on individual nutrient flows and on the microbial or non-microbial origin of duodenal contents. Parameter inputs for physical and chemical feed properties were identified that are improperly defined in extant models or susceptible to error. The description of these feed characteristics needs to be developed further and become identifiable for a wide range of dietary conditions.

Three ruminally and duodenally cannulated non-lactating Finnish Ayrshire cows were used to investigate ruminal and intestinal digestion of cell-wall carbohydrates by a combined in situ method. Five grasses cut at 10 d intervals were incubated in the rumen for 0, 6, 12, 24, 48, 72 and 96 h, and the undegraded residues were exposed to intestinal digestion. With advancing maturity of grass both the rate and extent of cell-wall digestion decreased. At early stages of growth the decreases were faster for the rate of digestion and at late stages of growth for the extent of digestion. Applying a passage rate of 0.02/h in one compartmental rumen model resulted in digestibility values markedly lower than typically observed in vivo. However, applying a rumen model incorporating a selective retention of particles and time-dependent release of particles from the non-escapable pool resulted in much higher digestibility values. Recovery of lignin after 96 h ruminal incubation with a subsequent mobile-bag incubation was very low (from 244 to 460 mg/g). Intestinal disappearance of neutral-detergent fibre (NDF) and hemicellulose decreased with advancing maturity of grass and with increasing length of preceding ruminal incubation period, i.e. with decreasing potential digestibility of the material. Disappearance of hemicellulose was much greater than that of cellulose for intact grasses but the difference diminished with increasing length of preceding rumen incubation period. On average, 195 mg/g of potentially digestible NDF disappeared from the mobile bags in the intestines. The post-ruminal digestion as a proportion of the total NDF digestibility varied between 0.034 and 0.058. Despite methodological problems both in ruminal in situ and intestinal mobile bag techniques, these methods can be used to investigate ruminal and intestinal cell-wall digestion and to partition cell-wall digestibility between ruminal and post-ruminal digestion providing that appropriate rumen models are used.

The effects of acidogenic conditions, a high S level and the addition of thiamin on the rumen microbial metabolism of thiamin were investigated in vitro in a semi-continuous fermenter (RUSITEC), using a factorial design. Acidogenic conditions were obtained by simultaneously increasing the starch: cellulose ratio and the amount of solid substrate fed, and by decreasing the buffering capacity of the liquid phase of the fermenter. S in the form of sulfate was supplied at two levels, one corresponding to a control amount of S (2 g/kg dietary DM), the second to an excess (5 g/ kg DM) which is sufficient to trigger cerebrocortical necrosis (CCN) when used in vivo. Acidogenic conditions decreased the pH of the fermenters, CH4 production and cellulose digestibility, increased the short-chain fatty acid production, but had no effect on thiamin production. The high S level enhanced the production of sulfide considerably, had no effect on the microbial metabolism of energy and N, and decreased thiamin production (326 ν. 266 nmol/d). The added thiamin was rapidly converted into phosphorylated compounds which largely decreased the apparent synthesis of this vitamin by the rumen microflora. The total thiamin flow was increased by added thiamin. In no case was thiaminase activity in the fermenter liquid phase significantly modified. The high level of S induced only a limited decrease of total thiamin flow. Consequently, it is unlikely that the investigated factors could be considered to be high risk factors for the thiamin-dependent CCN.

The effects of L-carnitine supplementation (50–500 mg/kg diet) of a practical layer diet, based on maize, soyabean and wheat, on the performance of laying hens and some indices of egg quality were studied for 8 weeks, using 65-week-old hens kept in cages. Albumen quality (albumen height and Haugh (1937) unit score) was improved, while yolk index and yolk colour score were not affected by dietary L-carnitine. The percentage of egg-white increased and that of egg yolk decreased in response to dietary supplementation of L-carnitine. Dietary L-carnitine did not influence laying performance (egg production rate, mean egg weight, daily feed intake, daily egg mass and feed conversion) or external egg quality measured by egg weight, egg-shape index or by eggshell quality, either measured directly as shell breaking strength or indirectly as shell weight, shell thickness or shell weight per unit surface area. Based on the results of the present study, L-carnitine had a beneficial effect on albumen quality and could modify the components of the edible part of the egg, during the late laying period.

The effects of a soluble NSP (fibre) concentrate (SFC) on plasma fibrinogen and plasminogen activator inhibitor-1 (PAI-1), serum and liver lipids and lipoproteins and glucose tolerance were compared with those of bezafibrate (BF), a lipid-lowering drug, in obese baboons (Papio ursinus) The basal diet was a high-fat (37% of total energy), low-NSP (12.4 g/d) Westernized diet, supplemented for 8 weeks with either 20 SFCg/baboon per d or 6.7 mg BF/kg body weight per baboon per d. SFC supplementation significantly lowered PAI-1, total serum cholesterol, HDL-cholesterol and circulating free fatty acid levels. BF significantly lowered total serum cholesterol, but unexpectedly raised serum triacylglycerol levels. Although not statistically significant, the mean liver tricacylglycerol concentration of baboons fed on BF was lower than that of baboons fed on SFC supplements. These results suggest that: (1) the mechanism of action of the two cholesterol-lowering treatments differ, with BF having a liver triacylglycerol-lowering effect and (2) the SFC had additional beneficial effect on fibrinolysis by lowering PAI-1 levels.

Non-physiological amounts of oral polyamines have been reported to induce precocious gut maturation in rat pups. The aim of the present study was to investigate organ distribution and metabolic fate of orally administered stable-isotopically labelled polyamines in rat pups. Pups received tetradeuterium-labelled putrescine (Pu-d4; 3 μmol), spermidine (Sd-d4; 5 μmol), spermine (Sp-d4; 3 μmol), or physiological saline twice daily on postnatal days 7–10 or 12–15. They were killed on days 10 and 15. We determined activities of ileal lactase (EC 3.2.1.23), maltase (EC 3.2.1.20), sucrase (EC 3.2.1.48) and diamine oxidase (EC 1.4.3.6) and established villus and crypt lengths. Polyamines and their labelling percentages in organs were determined by GC and mass fragmentography. Treatments did not affect growth rate, but caused lower weights of liver, kidneys and heart. Maltase activity increased, lactase decreased, whereas sucrase and diamine oxidase did not change. Villus and crypt lengths increased. Organ polyamine pools were labelled to different extents. Irrespective of the orally administered polyamine, all organs contained Pu-d4, Sd-d4 and Sp-d4. Administered Pu-d4 and Sd-d4 were recovered mainly as Sd-d4, whereas Sp-d4 was recovered as Sp-d4 and Sd-d4. Total polyamines in a caecum, colon and erythrocytes increased, but increases were only to a minor extent with regard to labelled polyamines. Our data confirm precocious gut maturation by exogenous polyamines. Putrescine appears to be the limiting factor. The exogenous polyamines were distributed among all investigated organs. They are not only used for the synthesis of higher polyamines, but also retroconverted to their precursors. Changes in erythrocyte polyamine contents suggest precocious stimulation of erythropoiesis.

To examine the effects of dietary docosahexaenoic acid (DHA) on the potential changes in endogenous lipid peroxidation in the liver and kidney, diets containing a fixed amount of vitamin E (VE; RRR-α-tocopherol equivalent; 134 mg/kg diet) and a graded amount of DHA at the levels of 0, 1.0, 3.4 and 8.7% of total dietary energy were fed to rats for 14 d (Expt 1). In Expt 2, diets containing a fixed amount of DHA (8.7% of total dietary energy) and a graded amount of VE at the levels of 54, 134 and 402 mg/kg were fed to rats for 15 d. In Expt 1 it was found that endogenous lipid peroxide contents of the liver and kidney, as measured by thiobarbituric acid value and chemiluminescence intensity, were higher, and their α-tocopherol contents lower than those of the controls, with a gradual increase and decrease in values respectively as the dietary DHA level increased (Expt 1). However, the contents of water-soluble antioxidants, i.e. ascorbic acid and non-protein-SH (glutathione), increased with increases in the dietary DHA level, while the Se-dependent glutathione peroxidase (EC 1.11.1.9) activities did not change or tended to be lower. When the graded level of VE was given to rats in Expt 2, lipid peroxide contents in the liver and kidney did not change significantly in response to the increasing levels of dietary VE, although their α-tocopherol contents were higher than control values, increasing with increases in the dietary VE levels. The lipid peroxide scavengers other than a-tocopherol changed similarly to those in Expt 1. The results obtained in Expts 1 and 2 indicate that DHA enhances the susceptibility of the liver and kidney to lipid peroxidation concomitant with higher levels of DHA in these tissues, as shown by the fatty acid composition. In addition, VE is unable to protect membranes of the liver and kidney rich in DHA from lipid peroxidation, even after ingestion of the highest level of VE. However, the liver lipid peroxide content of the group given the highest level of DHA was not as high as expected, based on the peroxidizability index which was calculated from the fatty acid composition of the liver lipid.

Weanling Wistar rats were fed on diets prepared from grain from areas deficient in I and Se where Keshan disease is endemic. Rats were divided into four groups, each of twelve rats, and received a diet supplemented with: I, Se, I + Se or nothing. At 8 weeks after weaning, myocardial α-glycerophosphate dehydrogenase (EC 1.1.1.8; α-GPD) activity and indices of Se and thyroid hormone status were determined. The group supplemented with iodine had increased plasma thyroxine levels. There was no difference in plasma triiodothyronine concentration between the groups but triiodothyronine levels in heart were reduced in the Se-supplemented group. Se supplementation increased myocardial glutathione peroxidase activity (EC 1.11.1.9) and the type I 5'-deiodinase (EC 3.8.1.4) activity in rat liver, but no type I 5'-deiodinase activity was detected in heart. α-GDP activity in heart was increased in the group supplemented with Se, I or both. There was a significant relationship (P < 0.05) between myocardial α-GDP activity and plasma thyroxine levels but not between α-GDP and myocardial glutathione peroxidase activity. The results indicate that iodine may be more important than Se in energy metabolism in the myocardium, which may give a new insight for the study of the aetiology of Keshan disease in areas where foodstuffs are deficient in both Se and I.