Vitamin D deficiency has been reported to result in impaired glucose tolerance and decreased insulin secretion when glucose is administered either intravenously or in-traperitoneally. The aim of the present study was to study oral glucose tolerance and glucose absorption in a vitamin D-deficient rat model, Oral glucose tolerance tests were carried out in vitamin D-deficient and control rats, and this was found to be unaltered in the deficient state. Intestinal absorption of glucose was drastically reduced in the deficient animal and was found to be due to a reduction in the sodium-dependent component of glucose trans-port. Thus the unaltered oral glucose tolerance in the vitamin D-deficient rat is probably due to impaired absorption of glucose.
The purpose of this study was to investigate the change in vitamin E level in both serum and red blood cells (RBC) during exercise and to clarify the effect of vitamin E supplementation. Ten young sedentary female subjects received 200mg D-α-tocopherol ac-etate daily for 1 wk after the initial exercise bout. After 1 wk of vitamin E supplementation, the same subjects repeated the same exercise. Before vitamin E supplementation, the α-tocopherol level in the serum (serum-α-tocopherol) did not change after exercise, but a signif-icant decrease in the α-tocopherol level in RBC (RBC-α-tocopherol) was observed after exer-cise (p<0.05). On the other hand, after vitamin E supplementation, the serum-α-toco-pherol level decreased significantly after exercise (p<0.05), while the RBC-α-tocopherol level was maintained after exercise. Furthermore, a negative correlation between the changes in serum- and RBC-a-tocopherol levels was observed only after vitamin E supple-mentation (r=0.667, p<0.05). The present results suggest that as RBC suffers oxidative stress, vitamin E in RBC is consumed to protect RBC from oxidative damage during exercise. These results also suggest that when there is a sufficient amount of vitamin E in the serum, vitamin E is shifted from the serum to RBC, resulting in a steady RBC-α-tocopherol level and a decrease in the serum-α-tocopherol level under oxidative stress such as exercise.
Radio-iron tests are frequently used to measure the bioavailability of different iron sources for food fortification. As the labeling procedures must be done under laboratory conditions, complementary studies should be carried out to evaluate the bioavailability of iron sources produced on an industrial scale. The iron bioavailability of SFE-171 (ferrous sulfate microencapsulated with phospholipids) was studied in previous reports using the compounds labeled with 59Fe and 55Fe; the results showed an iron bioavailability similar to that of ferrous sulfate. In the present work, the iron bioavailability of industrial SFE-171 was studied by the prophylactic-preventive method in rats using ferrous sulfate as the refer-ence standard. Elemental iron powder was also studied by the same method for comparative purposes. The liver iron concentration of each animal was determined at the end of the experiment in order to evaluate the influence of each iron source on the liver iron stores. Relative biological values of 98 and 34% were found for SFE-171 and elemental iron pow-der, respectively, while the corresponding relative liver iron concentrations were 104 and 45%. The results provided by the prophylactic-preventive method show that the iron bioavail-ability of industrial SFE-171 is similar to that of ferrous sulfate; these results are also in agreement to those obtained with the radioactive compounds. We can conclude that the SFE-171 obtained by industrial procedures for massive use in iron food fortification has the same bioavailability as that of the SFE-171 produced and labeled under laboratory conditions.
The synergistic effect of food additives or food colors on the toxicity of 3-amino-l, 4-dimethyl-5H-pyrido[4, 3-b]indole (Trp-P-1) was investigated using primary cul-tured rat hepatocytes. When hepatocytes from rats fed a standard diet were treated with a mixture of four major food additives (sorbitol, sodium L(+)-glutamate, benzoic acid, and propylene glycol) or a mixture of six typical artificial food colors (erythrosine, allura red, new coccine, brilliant blue, tertrazine, and fast green), the in vitro treated food-color mix-ture itself showed cytotoxicity; the reduction of cell viability and decreases in the activities of gluconeogenesis and ureogenesis. The food-color mixture enhanced cytotoxicity of Trp-P-1 obviously. We then investigated the effects of in vivo-dosed food additives or food colors on Trp-P-l-caused toxicity. Hepatocytes were isolated and cultured from rats fed a diet contain-ing a mixture of food additives or a mixture of food colors with half the amount of their re-spective acceptable daily intake for 4 wk. Trp-P-1 was administered to the hepatocytes at various concentrations for 12 h. Synergistic effects of in vivo-dosed food additives and food colors were not observed on Trp-P-l-caused cytotoxicity as estimated by a loss of cell viabil-ity and the reductions of DNA and protein syntheses. On the contrary, we have observed that in vivo administered food colors synergistically facilitated to reduce the activities of glu-coneogenesis and ureogenesis in Trp-P-l-treated hepatocytes. These results suggest that the daily intake of artificial food colors may impair hepatic functions such as gluconeogenesis and ureogenesis, when dietary carcinogens are exposed to the liver cells.
The influence of oxidized frying oil (OFO) on the guinea pig hepatic microso-mal xenobiotic-metabolizing enzyme system in the presence of different amounts dietary vi-tamin C was investigated. Weanling male guinea pigs were divided into four groups and were fed 15% oxidized frying oil diets supplemented with vitamin C at 300, 600, or 1, 500 mg/kg (experimental diets) or a control diet that contained 15% fresh untreated soy-bean oil with 300 mg/kg of vitamin C, respectively. After 60 d, guinea pigs were euthanized and phase I and phase II xenobiotic-metabolizing enzymes in the liver were determined. Compared with the fresh oil diet fed the control group, the relative liver weight was higher in the OFO-fed groups. Hepatic microsomal protein and cytochrome P450 contents were significantly higher in OFO-fed guinea pigs than in the control group. Both values increased in response to increased intake of vitamin C. The activities of phase II relative components, including UDP-glucuronyl transferase, UDP-glucuronyl dehydrogenase and β-glu-curonidase, of guinea pigs fed the OFO diets supplemented with 300 mg vitamin C/kg were significantly higher than those of guinea pigs fed the control diet. However, the phase II rel-ative components decreased with increasing vitamin C content in the diet. The results demonstrate that both dietary OFO and vitamin C in guinea pigs induce hepatic xenobiotic-metabolizing enzymes, but the level of induction is modulated by the dietary vitamin C level.
Using a vitamin E mixture extracted from palm oil, the tissue distribution of dietary tocotrienols and tocopherols was examined in rats and mice. Wistar rats (4-wk-old) were fed a diet containing 48.8mg/kg a-tocopherol, 45.8mg/kg a-tocotrienol and 71.4mg/kg γ-tocotrienol for 8 wk. Nude mice (BALB/c Sic-nu, 8-wk-old) and hairless mice (SKH1, 8-wk-old) were fed the same diet for 4 wk. α-Tocopherol was abundantly retained in the skin, liver, kidney and plasma of rats and mice. α-Tocotrienol and γ-tocotrienol were de-tected slightly in the liver, kidney and plasma, while substantial amounts of these to-cotrienols were detected in the skin of both rats and mice. The present study suggests that the skin is a unique tissue in respect to its ability to discriminate between various vitamin E analogs.
When type 1 diabetes mellitus was induced in rats by injecting streptozotocin, histidine decarboxylase expression was abnormally up-regulated in a transcriptional level, and 7 d after the injection, the enzyme activity was increased about 3-fold over the control (p<0.05). When the diabetic rats were administered with insulin for 3 d, the increased histi-dine decarboxylase activity returned to a normal level in addition to normalization of the plasma glucose level. The plasma gastrin level in the fasting state was also significantly ele-vated in the diabetic rats, and the insulin treatment normalized the level. In the diabetic rats, fasting gastric acid output increased significantly and gastric pH was lowered. These results suggest that the gastric histidine decarboxylase activity and plasma gastrin level are increased in connecion with the depletion of insulin in streptozotocin-induced diabetic rats, and gastric acid secretion is stimulated at a basal level, presumably due to increases in the concentrations of histamine and gastrin in oxyntic mucosa.