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Biomedical subjects

N Takeuchi

Publications and source records attributed to N Takeuchi.

At least 343 records · Page 19Linked to original sources
PubMed1977

Studies on uremic toxins: the identification and the determination of toxic effect by tissue culture method.

Uremic serum fractions obtained by Amicon XM-10 hollow fiber and membrane filtration was investigated using cytotoxicity in tissue culture by Rose's circumfusion system and by monolayer culture. The cytotoxic fraction was investigated with Elphor-Va 4, IR spectrometry, mass spectrometry, and NMR spectrometry for analysis of the true form of the substance. Remarkable cytotoxicity was observed in the small molecular fraction. Of the substances which may be surmised as uremic toxins, such as urea methylguanidine (MG), guanidinosuccinic acid, etc., only MG presented a similar cytotoxicity to this fraction. From the result of mass spectrometry, infrared spectrometry, and NMR spectrometry, it appeard that the electropositive substance included in the small molecular fraction was intimately associated with MG or one of its derivatives. The middle molecular fraction showed an inhibitory effect on cultured mouse liver glucokinase and human erythrocytic Na-K-dependent ATPase.

Adenosine Triphosphatases↗
PubMed1977

Stimulatory effect of Panax ginseng principles on DNA, RNA, protein and lipid synthesis in rat bone marrow.

Effects of extract fraction 3 and 4 from the root of Panax ginseng on bone marrow cells of the rat were investigated. Oral administration of fraction 3 and addition of fraction 4 in vitro stimulated DNA, protein and lipid synthesis in bone marrow cells. The stimulatory effect was reduced by pretreatment of cycloheximide. Single i.p. injection of fraction 4 also increased DNA and RNA synthesis. Numbers of mitosis were increased by oral administration of fraction 3. Extent of the increase was almost equal in both myeloid and erythoid. Numbers of total nucleated cells in bone marrow and reticulocytes in peripheral blood were significantly increased. The hematopoiesis-stimulating action of Panax ginseng and its mechanism of the action were discussed.

Animals↗
PubMed1976

Feed-back control of cholesterol synthesis in partially hepatectomized rats.

Partial hepatectomy caused a marked stimulation of cholesterol and fatty acid syntheses without affecting serum total cholesterol, total phospholipid and triacylglycerol concentrations of rats so far examined 48 h after the operation. Serum free cholesterol level, however, was increased by the treatment and the ratio of lysophosphatidylcholine to phosphatidylcholine was concomitantly decreased, suggesting the impairment of serum lecithin: cholesterol acyltransferase activity. The lipid content in the liver, especially triacylglycerol and ester cholesterol, was increased markedly by the operation. Feeding of a high cholesterol diet which elevated serum cholesterol and phospholipid levels to the partially hepatectomized rats, accelerated the accumulation of hepatic triacylglycerol and ester cholesterol by the partial hepatectomy. The weight of the regenerating liver was not influenced by cholesterol feeding, which suggested that cholesterol feeding did not inhibit the regeneration mechanism of the liver. The increase of cholesterol synthesis after partial hepatectomy was inhibited by cholesterol feeding. Therefore, it is conceivable that the negative feed-back control of cholesterol synthesis is induced by cholesterol feeding under the stimulated cell divisions of the liver after partial hepatectomy. It is suggested from the present data that a large amount of the cholesterol which is necessary for cell growth can be taken up from serum, when serum cholesterol concentration is high.

Acetates↗
PubMed1976

Cholestero metabolism in rats sensitive to high cholesterol diet.

There was great individual variation in the elevations of serum cholesterol concentrations in a Wistar strain of rats by the ingestion of a large amount of cholesterol, although their cholesterol concentrations were almost identical while under the feeding of a regular stock diet. Their serum total phospholipid and dextran precipitable beta-lipoproteins showed the same tendencies, but serum triglycerids concentration was not affected by the dietary supplement in both groups. So, the rats with the different elevation rates of serum cholesterol concentrations were divided into good, normo and poor responding groups to cholesterol ingestion by the degrees of the elvations and bred for several generations. Serum lipid levels in the descendants from hyperresponding rats were not different from those from hyporesponding rats during the observed period, when they were given a stock diet. However, the response of serum cholesterol level to oral cholesterol ingestion in the former was larger than that in the latter. Therefore, it is suggested that the susceptibility of serum cholesterol to cholesterol ingestion may be heritable from parents to their offsprings. By the results of the tracer experiments, it was demonstrated that neither hepatic cholesterol synthesis nor absorption was affected in hyperresponding rats. On the other hand, a half life of labeled cholesterol was prolonged in this selected group. The relative fractional turnover rate was 17.8 per cent in hyporesponding rats and 15.8 per cent in hyperresponding rats. Excretion of the radioactivity from labeled cholesterol into the bile in good responding rats with bile fistula was slower than that in poor responding rats. When 1 g per 100 g body weight of glucose was given to the rats after 40 hours fasting, hepatic cholesterol synthesis increased at the same rate in both groups of rats, but the induction of hepatic cholesterol 7alpha-hydroxylation in hyperresponding groups was slower than that in hyporesponding groups. The distribution rates of the radioactivities into livers seemed to be delayed in good responders after the labeled cholesterol was ingested orally.It means that some disturbances in cholesterol transport may exist which induce the metabolic abnormality in such animals. It was shown that cholesterol metabolism was impaired in aged animals as compared with young ones. Serum cholesterol concentrations were elevated in good responders more than in poor responders by aging. The inborn errors of cholesterol metabolism in such animals might be emphasized from the fact of the impairment of cholesterol metabolism by the aging process.

Aging↗
PubMed1976

Effects of synthetic progestational steroids on liver and serum lipids in rats.

Effects of norethisterone (NT) purified norethisterone (pure NT), norethynodrel (NE), medroxyprogesterone acetate (MAP), chlormadinone acetate (CMA) and desoxycorticosterone acetate (DOCA) on serum and liver lipid levels and serum lipoproteins were examined in both intact and estradiol-treated male rats. NT and NE caused a decrease in serum cholesterol and phospholipid levels, an increase in liver cholesterol level, no significant change in triglyceride levels of both serum and liver, with a significant change in serum lipoprotein patterns; a decreased in alpha- and beta-lipoproteins and a marked increase in pre beta-lipoprotein. Pure NT decreased serum cholesterol without causing any change in lipoprotein pattern. MAP, CMA and DOCA causee almost no effect on lipid levels in serum and liver, but CMA and DOCA increased alpha-lipoprotein and decreased beta- and pre beta-lipoproteins. An acute treatment with estradiol caused a decrease in alpha- and beta-lipoproteins and an increase in pre beta-lipoprotein with a decrease in serum lipid levels and an increase in liver lipids. By contrary, a chronic treatment with a marked hypercholesterolemia. This increase of alpha-lipoprotein in estradiol-treated rats was prevented by NT and NE, not affected or rather decreased by MAP but further increased with CMA and DOCA. These data suggest that the effects of synthetic progestational steroids on lipids are classified into two groups, 19-nortestosterone derivatives and 17alpha-hydroxyprogesterone derivatives including DOCA. The former caused a decrease in serum lipid levels with an increase of pre beta-lipoprotein and adecrease of alpha-lipoprotein. The latter caused almost no change or a slight increase in serum lipid levels with a decrease in pre beta-lipoprotein and an increase in alpha-lipoprotein, though it was not found in MAP.

Animals↗
PubMed1975

Effect of glucose administration on cholesterol and bile acid metabolism in rats.

Glucose administered to fasted rats caused a marked stimulation in hepatic cholesterogenesis and cholesterol 7 alpha-hydroxylation, and an increase in biliary excretion of cholesterol and total bile acids. The excretion of cholic acid was not incluenced during the first few hr after glucose administration, but was significantly increased after 5 hr. Chenodeoxycholic acid showed a similar change, but the increase was only ca. one tenth of that of cholic acid. The excretion of deoxycholic acid was markedly increased by 1 hr, but gradually decreased thereafter. Pretreatment with neomycin abolished the increase in deoxycholic acid by fasting and glucose administration. Other bile acid components showed no significant change. It thus was presumed that cholesterol endogenously synthesized in the liver was metabolized mainly to cholic acid. In contrast, exogenous cholesterol was metabolized mainly to chenodeoxycholic acid. During the period of the acute enhancement of cholic acid formation from the endogenous cholesterol, biliary excretion of deoxycholic acid was increased. This probably occurred through the depression of 7 alpha-rehydroxylation of deoxycholic acid, or through the enhancement of microbial formation of deoxycholic acid in the lumen, and through the increase of intestinal absorption.

Bile↗