Three experiments were conducted to estimate the effects of single intramuscular (IM) administrations of vitamin E on blood plasma and tissue concentrations of α-tocopherol in sheep. In Expt 1, plasma kinetics of α-tocopherol in sheep (n 30) were investigated following IM administration of three doses (ten sheep/dose) of DL-α-tocopheryl acetate, (20, 40 and 60 mg/kg live weight). Plasma profiles of α-tocopherol consisted of a lag phase followed by an apparent first-order absorption and elimination phase. The rate of absorption and elimination, as well as the lag phase, were independent of the dose, but the extent of absorption was directly proportional to dose. In Expt 2 (eighteen experimental and five control sheep), the animals were injected as in Expt 1 and were killed at 0, 80 and 176 h. Increases in α-tocopherol levels in organs were much higher than in plasma. Some tissues such as liver, spleen, lung and adrenal appeared to exhibit rapid absorption and elimination phases. The amount absorbed was proportional to the dose administered. Other organs such as heart, kidney and pancreas had a slow elimination rate. In Expt 3, D-α-tocopherol was injected IM into ten sheep at either 604 mg or 1208 mg. The mean hepatic α-tocopherol concentrations in both groups rose rapidly and after 4 weeks of dosing its concentrations were higher than the predosing levels. The increase in hepatic tocopherol concentrations were higher following 1208 mg dosing than 604 mg D-α-tocopherol. No simple relationship existed between plasma and hepatic α-tocopherol concentrations. This suggests a difference in body mechanisms controlling vitamin E in blood and liver.

The effect of dietary fibre and starch content on digestibility, microfaunal population and caecal function was investigated in a subterranean mole-rat, Heterocephalus glaber (Rodentia). Mole-rats were fed on a diet of either sweet potato (neutral-detergent fibre (NDF) 65 g/kg dry matter (DM), starch 638 g/kg DM) or carrot (NDF 157 g/kg DM, starch 258.7 g/kg DM) for 4 weeks. Daily intake and faecal output were monitored. Thereafter caecal microfaunal population, density and function were assessed using light and scanning electron microscopy and by measuring both gas and short chain fatty acid (SCFA) production. A 2.4-fold increase in fibre and 2.5-fold decrease in starch content resulted in a decrease in caecal DM content (390 g/kg). A concomitant dramatic decline (by 93%) in ciliate protozoa with a corresponding 2-fold increase in bacteria also accompanied this change in diet. Fermentative efficiency as indicated by gas production was 2.6 times greater on a carrot diet than on sweet potato. Microbial fermentation resulted in higher SCFA concentrations on the carrot diet, with a 42 % reduction in SCFA concentration on the sweet potato diet. Here, SCFA contributed 5.1 % of daily energy expenditure and this increased 5.0-fold on the carrot diet. Caecal micro-organism function, therefore, played an important role in the nutritional physiology of these naked mole-rats, and enabled maximum utilization of the food substrate.

The effect of vitamin A deficiency on the immune response to epizootic diarrhoea of infant mice (EDIM) rotavirus was studied in mice. The virus was given by oral dosing or by intraperitoneal injection. For oral challenge, weanling mice were fed on either a control or vitamin A-deficient diet ad lib. or pair-fed the control diet to the intake of the vitamin A-deficient group. A fourth group was fed on the vitamin Adeficient diet ad lib. for 10 weeks and then refed the control diet for 2 weeks. On day 77, mice were each given 30 μl EDIM rotavirus orally and the animals were killed and examined 1 week later. The delayedtype hypersensitivity (DTH) response to picryl chloride was measured as an index of cell-mediated immunity. For intraperitoneal challenge, weanling mice were fed on either the control diet or the vitamin A-deficient diet ad lib. or pair-fed the control diet to the intake of the vitamin A-deficient group. On day 77, mice were each injected intraperitoneally with 30 μl EDIM rotavirus and 1 week later antibody production was measured. In both experiments the body-weight, liver and serum vitamin A levels of the vitamin A-deficient group were significantly lower than the control or pair-fed groups. Following oral dosing the serum antibody levels specific to rotavirus were statistically significantly lower in vitamin Adeficient animals than the control or pair-fed groups. Vitamin A-deficient mice also showed an impaired DTH response compared with the control and pair-fed animals. Animals refed vitamin A for a short period showed a partial restoration of the antibody response. Following intraperitoneal challenge no statistically significant changes were observed in the serum antibody levels between any of the dietary groups. It is concluded that vitamin A deficiency impaired antibody production when rotavirus was given orally. Vitamin A deficiency also impaired cell-mediated immunity.

Iron absorption and daily loss of Fe were measured in riboflavin-deficient (B2-) Norwegian hooded rats and controls (B2+). Animals were fed on a test meal extrinsically labelled with 59Fe and whole-body radioactivity measured for 15 d. Riboflavin deficiency led to a reduction in the percentage of the 59Fe dose absorbed and an increased rate of 59Fe loss. All post-absorption 59Fe loss could be accounted for by faecal 59Fe, confirming that the loss was gastrointestinal. Fe concentrations and 59Fe as a percentage of retained whole-body 59Fe were higher in the small intestine of riboflavin-deficient animals than their controls, 14 d after the test meal. A separate experiment demonstrated that riboflavin deficiency was associated with a significant proliferative response of the duodenal crypts of the small intestine. These observations may explain the enhanced Fe loss in riboflavin deficiency.

The digestion by pigs of non-starch polysaccharides (NSP) in wheat and raw peas (Pisum sativum) fed in mixed diets was measured. In the four experimental diets, wheat was included at a constant 500 g/kg whilst peas contributed 0–300 g/kg and these were the only dietary sources of NSP. Separate estimates of digestibility for wheat and peas were obtained by using a multiple linear regression technique which also tested the possibility that the presence of peas might influence the digestibility of wheat NSP. There was little evidence of the latter and it was found that the digestibility of peas NSP (0.84) was considerably greater than that of wheat (0.65). The non-cellulosic polysaccharides (NCP) had twofold greater digestibilities than had cellulose for both foods with essentially all the peas NCP being digested. Faecal α-diaminopimelic acid concentration increased with feeding of peas, suggesting stimulation of bacterial biomass production in the large intestine using the readily fermented peas NSP. All three major volatile fatty acids produced by large intestinal fermentation were detected in jugular blood and increased significantly with increasing peas inclusion rate in the diet.

Sprague–Dawley rats were fed for 4 months on a control diet or a polyunsaturated-fatty-acid (PUFA)-deficient diet. The combined effects of iron overload (Fe dextran) or Fe deficiency (desferrioxamine) on carrageenan-induced granuloma were studied. PUFA deficiency induced changes in Fe metabolism, but no alterations in lipid peroxidation variables were observed. Inflammation implied an increase in lipid peroxidation, Fe storage and caeruloplasmin concentration, together with symptoms of anaemia. PUFA deficiency in inflamed rats gave rise to a lower inflammatory response (granuloma weight and prostaglandin E2 concentration) and ethane exhalation. Fe overload potentiated inflammatory and lipid peroxidation processes, whereas Fe deficiency decreased them.

An evaluation was made into the usefulness of ferrous fumarate as an iron fortificant for an experimental chocolate drink powder targetted to children and adolescents. Organoleptically ferrous fumarate was acceptable when the chocolate drink powder was reconstituted in milk or water that was heated to < 80°. Unacceptable colour changes occurred, however, when boiling milk or water were used. In human Fe absorption studies when the Fe compounds were added to the chocolate drink immediately before consumption, ferrous fumarate was 3.31 % absorbed compared with 2.82% for ferrous sulphate and 2.11 % for ferric pyrophosphate. When the Fe compounds were processed during the manufacture of the chocolate drink powder, the absorption of ferrous fumarate was 5.27 %, ferrous sulphate 2.62 % and ferric pyrophosphate 0.55 %. Ascorbic acid had little or no effect on the absorption of ferrous fumarate. It is concluded that food processing can influence the relative absorption of fortification Fe and that, if not reconstituted with boiling milk or water, ferrous fumarate could be a useful compound for the fortification of chocolate drink powders.

Brewer's yeast was grown on a defined medium containing tracer 51Cr with or without added chromium. The two batches of yeast contained 10 μg/g (high-Cr) or 80 ng/g (low-Cr). Extracts were prepared and fractionated. A third batch of yeast (third batch) was grown with added Cr, and fractionated. Rats were reared on either rat cubes (normal diet) or on a low-Cr diet (low-Cr), or on rat cubes with added cholestyramine (cholestyramine diet). Preparations of rat liver, both cell-free and intact hepatocytes, incorporated acetate-carbon into fatty acids and cholesterol. These processes were inhibited by a yeast fraction containing small, neutral, water-soluble compounds. The degree of inhibition was the same whether the liver came from normal rats or rats fed on the low-Cr diet. Similarly the inhibitory effect was found with identical amounts of extracts from low- or high-Cr yeasts. Therefore, Cr compounds do not appear to account for the inhibitory effects of brewer's yeast. Use of other substrates indicated that the site of inhibition of sterol synthesis was apparently between acetyl-CoA and mevalonate. One inhibitory substance was isolated from yeast and was found to be nicotinamide riboside. This may have been produced from NAD(P) during the preparation of yeast extracts, and it may be produced from dietary yeast supplements during digestion in vivo. Nicotinamide riboside may be partly responsible for the reported effects of yeast supplements on plasma lipids in humans.

The purpose of the present study was to evaluate the contribution of various substrates to glucose synthesis in isolated sheep hepatocytes, and more specifically to quantify the contribution of propionate to gluconeogenesis. Liver cells from fed sheep have a very high capacity for propionate utilization and conversion into glucose. The glucogenicity of lactate or amino acids was very low in hepatocytes from fed sheep, but was significantly increased in hepatocytes from starved animals. Amino acids such as alanine or glutamine were characterized by a substantial utilization towards ureogenesis, whereas their conversion to glucose was very low. Propionate utilization and conversion into glucose was inhibited by butyrate, ammonia and especially ethanol (by up to 80%). Ethanol promoted a striking accumulation of intracellular malate in hepatocytes incubated with propionate (reaching 14.9 μmol/g cell) and led to a depletion of phosphoenolpyruvate; ethanol inhibition could be counteracted by pyruvate. Propionate and butyrate enhanced ureogenesis from ammonia in ruminant liver cells but their effects were not additive. Propionate also elicited a marked increase in cellular concentrations of phosphoserine and serine, particularly in the presence of ammonia; such effects could influence phospholipid metabolism in the liver. These findings emphasize the contribution of propionate, compared with the other glucogenic substrates, to glucose synthesis in ruminants and point to the possibilities of modulation of the glucogenicity of propionate by various substrates which may be present in portal blood.