We have investigated the effects of maternal diets low in fat or protein, or restricted in total food intake on vitamin A transfer from the dam to her pups. When animals were fed on diets moderately restricted in fat or protein, minimal differences in milk, serum, and liver vitamin A concentrations were observed compared with animals fed on a control diet. In a second study, dams were fed on diets more severely restricted in protein, or fat, or both, or were fed on a control diet equal to 50% of the intake of control rats but containing an equal amount of vitamin A. The quantity of milk obtained from these more severely restricted dams' nipples or the pups' stomachs was greatly reduced; however, there were no differences in milk vitamin A concentration. Body-weight, liver weight, and total liver vitamin A stores of undernourished pups were just half those measured for control pups, although serum vitamin A and serum retinol-binding protein were nearly normal in concentration. We conclude that (a) moderate restrictions in fat or protein in the maternal diet are insufficient to affect transfer of vitamin A to the suckling pup; (b) further dietary restrictions could cause decreased milk production with little change in milk vitamin A concentration and, hence, (c) the neonates' hepatic retinol accumulation during the suckling period is markedly reduced when maternal diets are severely deficient in fat or protein or of normal composition but restricted in amount.

Weanling mice were fed on a control diet ad lib., a vitamin A-deficient diet ad lib. or pair-fed to the intake of the vitamin A-deficient group. Vitamin A deficiency was induced by 63–70 d of age. On day 77 mice were given 30 μl rotavirus/mouse orally and examined histologically 1 week later. There were no changes in relative liver weight in any of the groups, but following infection animals deficient in vitamin A showed a significant increase in spleen weight compared with the other groups. The relative weight of the thymus was reduced by vitamin A deficiency, in both non-infected and infected animals. The histology of the spleen, thymus and small intestine was similar in all three dietary groups before infection. The number of goblet cells per duodenal villus in vitamin A-deficient animals was significantly lower than that of control and pair-fed animals. In the small intestine of vitamin A-deficient animals, rotavirus infection caused dramatic changes to the mucosa, with almost complete destruction of the tips of the villi, but control and pair-fed animals had normal villi. It is concluded that although rotavirus infection and vitamin A-deficiency cause few changes alone, in their action together there is significant destruction of the mucosal barrier of the small intestine.

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.

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.