Brewer's yeast was grown on a defined medium containing glucose, ammonia, salts and vitamins plus tracer 51Cr without (low-Cr) or with (high-Cr) carrier Cr. The two batches of yeast differed by more than 100-fold in Cr content, containing 80 ng and 10 7mu;g Cr/g dry yeast respectively. Extraction and fractionation procedures were designed to isolate Cr complexes with properties similar to those reported for glucose tolerance factor. After weaning, rats were reared on rat cubes (normal diet) or on a diet containing less than 0.1 μg Cr/kg (low-Cr diet), or on the low-Cr diet supplemented with Cr (1 mg Cr/kg). Hepatocytes from these rats were incubated with [U-14C]glucose and incorporation of 14C into glycogen was measured. Incorporation of glucose-C into glycogen was enhanced by some yeast fractions in the presence of insulin, but had less effect in the absence of insulin. No difference could be detected between the responses to fractions from high- or low-Cr yeast extracts, or between responses by hepatocytes from animals fed on normal or low-Cr diets with or without Cr upplementation. Glycogen synthetase (EC 2.4.1.11) activity (total and percentage in the a form) was similar in hepatocytes isolated from animals on the normal and low-Cr diets. Those yeast fractions which enhanced the response to insulin in the 14C-incorporation experiments also enhanced the percentage of the enzyme in the a form in the presence of insulin, but not in the absence of insulin. The presence in yeast extracts of material which enhances the response to insulin by hepatocytes may help to explain the reported beneficial effects of dietary yeast supplements on glucose tolerance.

The fate of radiotocopherol was studied in plasma and tissues of sheep at various intervals after injection of single intravenous doses of 3H-labelled D-α-tocopherol. Plasma samples were taken at regular intervals after dosing and selected tissues were taken from all sheep after slaughter and assayed for radioactivity and D-α-tocopherol. Sheep were killed in groups of five at 24, 72, 96, 272 and 432 h post-dosing. Plasma profiles were characterized as a sum of three exponential terms. A principal component analysis of tissue concentrations was carried out to identify tissues with parallel profiles of log (disintegrations/min per μg) over time. Five groups of tissues with distinct uptake and elimination processes were identified. The D-α-tocopherol in the liver and heart appeared to be consistent with the post-distributive kinetics of a highly perfused shallow compartment, while lung kinetics appeared to reflect a non-linear kinetic process. The third group, which included the spleen, neck brachiocephalicus muscle and pancreas, had depletion rates parallel to those of plasma for 24–272 h, but slower decreases than plasma over 272–432 h. Hip gluteus muscle and kidney comprised a fourth group, with depletion parallel to plasma rates for 24–96 h but progressively slower than plasma decreases over 96–272 h. Adrenal kinetics resembled the fourth group, but had a more rapid decrease in specific activities over 24–72 h.

Plasma and erythrocyte (RBC) tocopherol-isomer concentrations were determined serially in forty-two premature infants (25–35 weeks gestation) from birth to 8 weeks of age. For comparison purposes vitamin E status was also determined in six term infants over the first 8 d following birth and in a group of thirteen adult volunteers. Vitamin E intakes in term and preterm infants were calculated from recorded food intakes and blood transfusions. In term infants plasma vitamin E concentration rose from 1.9 mg/l (day 1) to 8 2 mg/l by day 8. In comparison preterm plasma vitamin E concentration, 0.3 mg/l (day I), did not change appreciably by day 8 (0.7mg/l). Likewise RBC vitamin E concentration increased in term infants from 1.3 mg/l (day 1) to 2.7 mg/l (day 8), while in preterm infants it remained unchanged, 1.5 mg/l (day 1) v. 1.3 mg/l (day 8). Over the 3 weeks following birth, RBC vitamin E concentrations in the premature infants increased to adult values, while plasma vitamin E concentration did not reach the adult range until 8 weeks post-term. These slow changes in plasma vitamin E status occurred even though the vitamin E intake of these infants was similar to that proving adequate for term infants.

The present study was designed to examine the effects of various levels of fructose in a copper-deficient diet on some of the signs of Cu deficiency in the rat. Weanling male rats were randomly assigned to one of five diets which contained 0.6 μg Cu/g diet and 627 g carbohydrate/kg which was (g/kg): 627 fructose (diet 100); 470 fructose, 157 starch (diet 75); 313.5 fructose, 313.5 starch (diet 50); 157 fructose, 470 starch (diet 25); or 627 starch (diet 0). Rats ate their respective diets for either 2 or 5 weeks. There was a significant linear inverse response of body-weight (P < 0.0001), packed cell volume (p < 0.0001) and erythrocyte superoxide dismutase (EC 1.15.1.1) activity (P < 0.008) to increasing levels of dietary fructose and a direct linear response of plasma cholesterol (P < 0.05) and blood urea nitrogen concentrations (P < 0.001) to increasing levels of dietary fructose. Liver, kidney and pancreatic Cu concentrations decreased in a dose-response manner as the level of dietary fructose increased. In general, if fructose was included in the diet the signs of Cu deficiency were exacerbated in a dose-response manner.

Rats given a low-fibre diet based on boiled white rice developed symptoms of severe vitamin K deficiency within 23 d. Inclusion of autoclaved black-eye beans (Vigna unguiculata) in the diet prevented the bleeding syndrome. To test the hypothesis that deficiency resulted from low phylloquinone intake exacerbated by inadequate production of menaquinones by the enteric bacteria, a follow-up experiment was carried out in which groups of rats were given an all-rice diet, a rice+beans diet or a stock diet. Rats on the allrice diet had significantly lower faecal concentrations of the main menaquinone-producing bacterial species (Bacteroides fragilis and Bacteroides vulgutus) than animals on either of the other two diets. This coupled with the much lower faecal output on this diet suggests that total menaquinone production was low for the all-rice diet. The alterations in faecal flora were associated with several significant changes in caecal metabolism. Rats given the stock diet had much shorter caecal transit times and a considerably greater proportion of butyric acid in volatile fatty acid end-products than did rats on either of the other two diets.

To examine how fat might influence the metabolic effects of tumour necrosis factor α (TNFα), human recombinant TNFα was given intravenously to rats that had been fed for 12 weeks on diets containing (g/kg) 200 maize oil or 190 coconut oil+10 maize oil. Rectal temperature and tissue composition measurements were made 8 and 24 h after injection. Ambient temperatures of 20° and 25° were employed to accentuate rectal temperature changes. Doses of 30 and 300 μg TNFα/kg body-weight were given, and brought about depression of serum zinc and albumin and elevation of copper. Muscle protein content was decreased and liver protein and Zn content enhanced by TNFα. Serum Zn and liver Zn content were negatively correlated 8 h after injections. Hypothermia developed within 1 h of injection. All responses except the rise in serum Cu and gain in liver Zn were more intense at the higher than at the lower dose of TNFα. Hypothermia was exacerbated by an environmental temperature of 20°. The coconut-oil diet blunted the hypothermia and likewise the changes in serum albumin and Cu content 8 h after injections and in muscle and liver protein after 24 h. Changes in eicosanoid metabolism may be involved in the modulatory effects of the coconut-oil-enriched diet.