Journal of Nutritional Science and Vitaminology
Online ISSN : 1881-7742
Print ISSN : 0301-4800
ISSN-L : 0301-4800
Volume 20, Issue 3
Displaying 1-9 of 9 articles from this issue
  • Toru KOMAI, Kenji KAWAI, Hideyo SHINDOI
    1974 Volume 20 Issue 3 Pages 163-177
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The tissue accumulation method was ascertained to be a more suitable method for studying the intestinal absorption mechanism in vitro than the everted sac method. By means of the tissue accumulation method, the absorption mechanism of thiamine from the rat small intestine was investigated. The ratio of intracellular to extracellular concentration was found to exceed unity with respect to free thiamine, indicating that thiamine is transported against a concentration gradient. Then, thiamine uptake by the intestinal segments was saturable and dependent on the incubation temperature. The transport required metabolic energy and was inhibited by pyrithiamine and chloroethylthiamine competitively. These evidences indicate that thiamine is absorbed from the rat small intestine by active transport.
    Chloroethylthiamine, which has no inhibitory effect on thiamine pyro-phosphokinase, inhibited thiamine transport. Moreover, thiamine pyrophosphokinase was scarecely detected in microvillous membrane. The longitudinal distribution of thiamine pyrophosphokinase activity along the digestive tract did not coincide with that of the activity of thiamine uptake. These results indicate that there is a carrier system for thiamine transport which is not dependent upon the phosphorylation process in the rat small intestine.
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  • Toru KOMAI, Hideyo SHINDO
    1974 Volume 20 Issue 3 Pages 179-187
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The structural specificity of the thiamine transport system in the rat small intestine was examined by studying the ability of thiamine analogues to inhibit the unidirectional influx of 35S-thiamine from medium to everted ring segments of the rat small intestine.
    The results indicated that the amino group and the quarternary nitrogen atom are both required for the transport of thiamine by the rat small intestine, and that 2'-methyl and 5-hydroxyethyl groups significantly influence the binding of thiamine molecule to the carrier. The C-2 position of thiazole moiety, which is an active site of coenzyme reaction of thiamine pyrophosphate, seems to play no role in thiamine transport. The thiamine transport system was found to be different from the sugar and amino acid transport systems.
    A conceptual model of the thiamine binding to the carrier was presented.
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  • Toru KOMAI, Hideyo SHINDO
    1974 Volume 20 Issue 3 Pages 189-196
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    Thiamine transport by the red blood cells of rats was investigated at a physiological concentration of thiamine. The transport rate became large in accordance with the decrease of the initial thiamine concentration in the medium. Pyrithiamine and chloroethylthiamine inhibited this transport but oxythiamine did not. The examination of counter flow showed that thiamine efflux from the red blood cells after preloading was accelerated by thiamine added in the medium. However, the metabolic energy was not required for the thiamine transport by the red blood cells. This evidence indicates that thiamine is taken up by facilitated diffusion by the red blood cells of rats at a physiological concentration of thiamine.
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  • Sada OHGURI
    1974 Volume 20 Issue 3 Pages 197-202
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The effect of tryptophan deficiency on the urinary excretion of tryptophan and niacin metabolites and riboflavin, and on nitrogen balance has been examined in rats.
    The excretion of xanthurenic acid decreases, and the excretion of N1-methylnicotinamide (MNA) slightly increases when tryptophan is deficient. But the increase in MNA excretion was not statistically significant, perhaps owing to the scatter of the data.
    Decrease in the excretion of N-methyl-2-pyridone-5-carboxamide (pyridone) is as low as 1/2 to 1/20 of the control level when tryptophan is deficient. The excretion of riboflavin increases when tryptophan is deficient.
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  • Shin-etu ONO, Kin-ya KAMEDA, Yasushi ABIKO
    1974 Volume 20 Issue 3 Pages 203-213
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The consecutive changes in blood concentrations and the urinary excretion of free and bound pantothenic acid were studied after oral and intravenous administration of pantethine (21.6 μmoles/kg) to rats. The results were compared with those obtained after administration of Ca-pantothenate (21.6 μmoles/kg).
    The concentration of total pantothenic acid in blood was significantly higher in the pantethine group than in the Ca-pantothenate group after oral administration of vitamins. The maximal concentrations were observed at 2-4.5 hr after ingestion in both groups. The excretion rates of total pantothenic acid in 24-hr urines were 29±3 % of the dose and 18±2% in the pantethine and the Ca-pantothenate groups, respectively. These findings indicate that pantethine was more absorbable through the gastrointestinal wall of the rat than Ca-pantothenate. No significant difference was, however, found in the amounts of bound pantothenic acid in blood between these two groups. Pantethine was found to be hydrolyzed, to some extent, to pantothenic acid by an enzyme during passing the intestinal mucosa. After an intravenous injection of pantethine, about 50% of total pantothenic acid in blood was pantethine and the rest was free pantothenic acid, while little bound pantothenic acid was detected after injection of Ca-pantothenate. The decrease in total pantothenic acid in blood was significantly delayed in the early period after injection in the pantethine group when compared with that of the Ca-pantothenate group, although both the vitamins were almost completely eliminated in 24-hr urines after injection.
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  • Tokuji HOSOTANI, Akira YOSHIDA
    1974 Volume 20 Issue 3 Pages 215-225
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    The accumulation of lipid in the liver was observed in rats fed a non-protein diet supplemented with methionine, but further supplement of threonine partially prevented liver lipid accumulation. Supplements of leucine, phenylalanine or histidine slightly lowered the liver lipid accumulation of rats fed the nonprotein diet containing methionine. On the other hand, free fatty acid in the plasma was not changed when rats were fed the nonprotein diet supplemented with methionine. No difference Was observed in the plasma lipoprotein of rats fed a non-protein diet supplemented with or without methionine. However, the threonine supplement increased the total esterified fatty acid in the plasma lipoprotein (d<1.006) of rats fed a nonprotein diet containing methionine. A slight decrease was observed in the β-lipoprotein of rats fed the nonprotein diet supplemented with methionine. When injected with Triton WR-1339, the total esterified fatty acid content remarkably increased in the plasma of rats fed the nonprotein diet supplemented with methionine as well as the nonprotein diet, and the plasma β-lipoprotein of Triton WR-1339 treated rats was also increased in both groups. Therefore, it was assumed from the results that the transport of lipid from liver into blood is not inhibited in this type of fatty liver. At present, the cause of the fatty liver due to methionine supplementation to a nonprotein diet is not clear. However it seems un-likely that the inhibition of the lipoprotein transport from the liver to the blood plasma is the main reason for it.
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  • Yukihiro NAKABOU, Chiyo OKITA, Yasuo TAKANO, Hiroshi HAGIHIRA
    1974 Volume 20 Issue 3 Pages 227-234
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    In alloxan diabetic rats both the weight and total nitrogen content of the small intestine increased markedly. The intestinal enlargement was caused by increased food intake and was due mainly to hyperplasia with some hypertrophy. The intestine of diabetic rats fed on a restricted diet did not become larger.
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  • Kaneyuki SOHODE, Tadashi OGAWA, Setsuro MATSUSHITA
    1974 Volume 20 Issue 3 Pages 235-237
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
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  • Kiyoshi TSUKIDA, Kayoko SAIKI, Masayoshi ITO, Hiroko NAKAMINAMI, Mamik ...
    1974 Volume 20 Issue 3 Pages 239-241
    Published: 1974
    Released on J-STAGE: April 28, 2009
    JOURNAL FREE ACCESS
    DANNENBERG and HEBENBROCK obtained a fluorescent hydrocarbon, C27H34, by refluxing vitamin D3 with chloranil in anisole (bp 155.5°C) for 1 hr (35% yield), to which a structure possessing the styryl indene chromophore was assigned (1). During the course of our study on a fluorometric determination of vitamin D, we found this reaction to be unsuited for analytical purposes mainly because of its drastic reaction condition. We wish to report a very easy method of aromatization of vitamin D under extremely mild reaction conditions, and to emphasize the biosynthetic significance of this reaction.
    Treatment of vitamin D2 (I) in acetone with an equimolar amount of N-bromosuccinimide at room temperature for a period of 10 min led to a complete disappearance of the initial vitamin. Extraction of the diluted aqueous acetone solution with n-hexane gave a reaction mixture consisting principally of the two fluorescent components A and B, in approximately 3:1 proportion (2) as estimated by NMR (3). No other reaction products were detected on gas chromatographic tracings (4). Successive column chromatographic separation on silica gel, using n-hexane, afforded the ingredient A in a pure state (5). On the basis of the following data and of a comparative examination with the known vitamin isomers such as isovitamin D2 (II) and isotachysterol2 (III), the structure (IV) has been determined unequivocally for the compound A, and (V) was assigned tentatively to the compound B.
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