Studies on Riboflavin Tetranicotinate

Kotaki, Akira; OKUMURA, MISAO; NAKAGAWA, YOKICHI; Yagi, Kunio

doi:10.5925/jnsv1954.15.43

Cited by 3 publications

(3 citation statements)

References 9 publications

(12 reference statements)

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“…This may be due to the fact that 95% of the newly accumulated fat is composed of oleic, palmitic and palmitoleic acids (10) that are considered to be relatively resistant to peroxidation. The present result is, however, different from the previously observed result in the fatty liver induced by nutritional imbalance (11) The other finding which is different from the previously observed result in the experi ment of fatty liver induced by nutritional im balance, is that in this case the actions of choline and myoinositol are not synergistic but likely to be antagonistic, in preventing fat accumulation in the liver. Although fur ther investigations are required to solve the meaning of these different observations, it should be stressed here that the lipotropic mechanisms of choline and myoinositol can not always be explained by only the hypo thetical view of Agranoff and Fox (12).…”

Section: Tablecontrasting

confidence: 99%

Studies on Myoinositol

Kotaki¹,

OKUMURA²,

HASAN³

et al. 1970

J. Vitaminol

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Induction of fatty liver in rats by feeding on diets containing 1.5% orotic acid for 7 days, was accompanied with the increase in the lipid TBA value and with the decrease in the lipid phosphorus concentration.However, fat accumulation was prevented by injecting 30mg of myoinositol or choline sub cutaneously every day during the experimental period.The prevention was found to be about 20-50%with myoinositol and about 90% with choline. However, the effects of choline and myoinositol were not synergistic; the effect due to the injection of both choline and myoinositol was rather close to the effect of myoinositol alone.The increase in lipid TBA value and the decrease in lipid phosphorus concentration were also found to be prevented by injecting these lipotropic factors.

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Section: Tablecontrasting

confidence: 99%

Studies on Myoinositol

Kotaki¹,

OKUMURA²,

HASAN³

et al. 1970

J. Vitaminol

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“…This effect disappeared within 6 hr. A similar hypo thesis was proposed by Yagi et al (6)(7)(8). They suggested that phosphatidylinositol plays an important role in the release of beta-lipoprotein in fatty liver induced by a low-protein diet.…”

supporting

confidence: 69%

Effect of Orotic Acid on the Distribution of Phosphatidylcholine [32P]

Negishi¹,

Aizawa²

1975

Japanese Journal of Pharmacology

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Triglyceride accumulation in the liver can be brought about by a disease state in man, and by the administration of a large variety of agents (1, 2). A block in the release of hepatic beta-lipoprotein into blood stream appears to be responsible for the development of a number of experimentally induced fatty liver conditions (3).Our previous results demonstrated that a decreased release of beta-lipoprotein from liver slices in rats fed orotic acid was restored by the addition of phosphatidylcholine. It was further found that phospholipid has a curative effect on fatty liver induced by orotic acid or ethionine. These findings suggest that phospholipid is an important factor in the normal release of beta-lipoprotein. Accordingly, it is of interest to examine the fate of ingested phosphatidylcholine. The present experiments were done to examine the distribution of phosphatidylcholine [32P] in rats fed orotic acid.Female Wistar strain rats weighing 180 to 210 g were first fed a semisynthetic diet (4) for 2 days. Control rats were given a semisynthetic diet alone. Groups of animals then were put on a dietary supplement of I ;o orotic acid for 7 days after which 0.373 or 0.824 /iCi of phosphatidylcholine [32P] to which was added 14 mg of non-radioactive phosphatidyl choline as carrier in 0.5 nil of saline solution (1.91 or 4.23 /tCi/Kg body weight) was in jected intraperitoneally. At the indicated time after administration of the phospholipid, the rats were sacrificed by heart puncture under ether anesthesia. Tissues were removed, homogenized with ice-cold 5 trichloroacetic acid, and centrifuged. The precipitate was washed twice with ice-cold trichloroacetic acid. Lipids were then extracted once with 80% ethanol, once with 100% ethanol, twice with chloroform-ethanol (1 : 1, by vol.), and once with ether. Trichloroacetic acid was added to the serum, and centrifuged. Serum lipids were then extracted with chloroform-methanol (2: 1, by vol.). Radioactivity of acid-soluble and lipid fraction was determined in a liquid scintillation spectrometer using dioxan and toluene-phosphor solution, respectively.Phosphatidylcholine [32P] was prepared as follows: Liver slices were incubated with 1.25 mCi orthophosphate [32P] per ml of Krebs-Ringer bicarbonate buffer at 37' in 02 CO2 (95: 5, by vol.) for 5 hr. Lipids were extracted as described above. Phosphatidyl choline was separated by paper chromatography according to the method of Marinetti et al. (5). The specific radioactivity of the prepared phosphatidylcholine [32P] was 18.4 1eCi/

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“…It is more likely that the pro tein synthesis in the endoplasmic reticulum is totally decreased, and this may be, even though partly, explained by the fact that the level of lipoperoxide, which is toxic for various enzymes (27), is high in the fatty liver of this kind (28).…”

Section: Discussionmentioning

confidence: 99%