[Amount of cholesterol in foods].
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Cholesterol↗
Biomedical subjects
H Itakura
Publications and source records attributed to H Itakura.
[Reference for diagnosis of hyperlipidemia--characteristics and significance of Japanese guideline].
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Cholesterol, LDL↗
Generation, characterization, and kinetics of triplet Di[1,2,3,4,5,6, 7,8-octahydro-1,4:5,8-di(ethano)anthryl]carbene.
The title carbene has been generated by photolysis of the corresponding diazo precursors and studied by spectroscopic means, i. e., electron paramagnetic resonance (EPR) and UV/vis spectroscopy in matrixes at low temperature and laser-flash photolysis in solution at room temperature, with the product analysis. The results are compared with triplet di(2,3,5,6-tetramethylphenyl)carbene, an open-chain counterpart, which revealed that bicycloalkyl groups are acting as a fairly good kinetic protector for the triplet carbene as opposed to the open-chain counterpart. The formation of all-hydrocarbon triplet carbenes having a half-life over a second under normal conditions was realized for the first time. Effects of para-substituents on the structure and reactivities of the carbene are also investigated and discussed in terms of polar and spin electronic effects.
Journal Article↗
Generation and characterization of triplet anthryl(aryl)carbenes.
The title carbenes where aryl groups are phenyl, 2,4, 6-trimethylphenyl, and octahydro-1,4:5,8-di(ethano)anthryl were generated for the first time by irradiation of the corresponding diazo precursors and fully characterized by ESR in a rigid matrix at low temperature. It has been demonstrated that anthryl groups can act as excellent reservoirs for the unpaired electrons as well as relatively effective kinetic protectors for carbene.
Journal Article↗
Primary rectal teratoma: EUS features and review of the literature.
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Aged↗
Gene expression related to cholesterol metabolism in mouse brain during development.
Although a large amount of cholesterol is known to be needed for brain maturation and differentiation, cholesterol metabolism during these periods remains unclear. To elucidate the developmental regulation of cholesterol metabolism in the brain, we investigated the expression of 3-hydroxy-3-methyglutaryl-coenzyme A (HMG-CoA) reductase (EC 1.1.1.34), low-density-lipoprotein (LDL) receptor and very-low-density-lipoprotein (VLDL)/apolipoprotein E (apo E) receptor (VLDL receptor) using RNase protection assay (RPA) to quantitate mRNA levels in mouse brain, liver and kidney during development. Messenger RNA levels of HMG-CoA reductase in the brain decreased with age, and those levels at -5 (5 days before birth) and 5 days after birth were significantly higher than the control level of adult mice. The period from -5 to 5 days might correspond to stages of active biogenesis of the membranes of brain cells. The mRNA level of HMG-CoA reductase in the liver was also high at -5 days; a finding that correlated with cell proliferation. On the other hand, mRNA levels of the LDL and VLDL receptors in the brain did not change markedly during development. These results suggest that de novo cholesterol biosynthesis in brain cells plays a major role in the supply of cholesterol to the developing brain, rather than the uptake of cholesterol from serum lipoproteins through lipoprotein receptors.
Aging↗
Spermatic cord metastases from gastric cancer with elevation of serum hCG-beta: a case report.
Spermatic cord metastases from gastric cancer are rare. We here document a case involving a gastric cancer that mimicked primary testicular tumor because of elevation of the serum human chorionic gonadotropin-beta (hCG-beta). The possibility of metastasis or recurrence of prior malignancies should therefore be considered when the clinical features described here are encountered, although elevation of hCG-beta is rare with tumors other than those in testis.
Biomarkers↗
Dietary diacylglycerol suppresses accumulation of body fat compared to triacylglycerol in men in a double-blind controlled trial.
We examined the effects of the long-term ingestion of dietary diacylglycerols (DG) in a double-blind controlled study of human lipid metabolism. Healthy men (n = 38; aged from 27 to 49 y, body mass index (BMI) ranging from 21.8 to 27.4 kg/m(2)) completed the study. To accustom the subjects to the test diets prior to the experiment, they were supplied with test diets of triacylglycerol (TG) oil for 4 wk (control period). The test oils (10 g/d) were included in bread, mayonnaise or shortbread and served for the breakfast. The target for total lipid intake was 50 g/d (15 g for breakfast, 15 g for lunch and 20 g for dinner) throughout the study. The subjects were then divided into two groups so that mean BMI and the hepatic fat content, determined by computed tomography, for each group were not different. One group (DG group) consumed test meals containing DG-rich oil (10 g/d) while the other group (TG group) consumed the same meal as during the control period. Ten grams of the DG-rich oil contained 5.5 g 1,3-DG, 2.5 g 1,2-DG and 2 g TG. The actual lipid intake during the study was 43 g/d. Body weight, BMI and waist circumference decreased in both groups at the end of the test period of 16 wk. However, the magnitudes of decreases in these variables were significantly greater in the DG group than in the TG group. Decreases of total fat, visceral fat area and subcutaneous fat area of the abdominal traverse images of computed tomography in the DG group were also significantly greater than those in the TG group. Hepatic fat content decreased significantly in the DG group while no change was observed in the TG group. Serum lipid concentrations (TG, total cholesterol, free fatty acid) and related metabolites (glucose, insulin, total ketone body) did not change significantly in either group. Thus, in contrast to TG, DG apparently suppressed accumulation of fat and possibly reduces the risk of diseases associated with visceral fat obesity.
Abdomen↗
Antioxidant effects of polyphenols in chocolate on low-density lipoprotein both in vitro and ex vivo.
Cacao is rich in polyphenols such as (-)-epicatechin, and a colored component of cacao (cacao-red) is polyphenol, which is an antioxidant. These properties stimulated an investigation of the effects of cacao liquor polyphenols (CLP) on low-density lipoprotein (LDL) oxidation. The 2.2 '-azobis(4-methoxy-2,4-dimethylvaleronitrile) (AMVN-CH2O)-induced oxidizability of LDL was assessed by monitoring the absorbance at 234 nm. In vitro. 0.1-0.5 mg/dL CLP prolonged the oxidation lag time of LDL in a dose-dependent manner. Compared with the controls, it was prolonged 1.7-fold in the presence of 0.1 mg/dL CLP, 2.9-fold at 0.2 mg/dL, 3.8-fold at 0.3 mg/dL, 5.4-fold at 0.4 mg/dL, and 6.4-fold at 0.5 mg/dL. Furthermore, we enlisted 13 male volunteers to consume 35 g delipidated cocoa. Venous blood samples were taken before and at 2 h and 4 h after consuming the cocoa. The oxidation lag time of LDL before cocoa ingestion was 59.0 +/- 6.3 min, but it was prolonged at 2 h after cocoa (68.3 +/- 6.0 min); before returning to the initial lag time (61.7 +/- 5.7 min) before consumption. Thus we have shown that cocoa inhibited LDL oxidation both in vitro and ex vivo.
Adult↗
Antioxidative effects of Choi-oki-to and its ability to inhibit the progression of atheroma in KHC rabbits.
Agents which inhibit the oxidative modification of low density lipoprotein (LDL) have been thought to be helpful in preventing the formation of atherosclerotic lesions; the so called "oxidation hypothesis". To test this hypothesis, we examined the antioxidative activities of 127 Kampo medicines in vitro and their inhibitory effects on the development of atheromatous plaque formation in KHC rabbits, a model of spontaneous familial hypercholesterolemia. Some of the 127 Kampo medicines showed scavenging or antioxidative effects equal to or stronger than those of probucol in vitro. Choi joki to, which had the strongest antioxidative effects on LDL in vitro, was chosen for a study in vivo. After 24 weeks, 1 g/kg of Choi joki to successfully inhibited the progression of atherosclerotic lesions in KHC rabbits (P < 0.01). Further investigations regarding the antioxidative effects of Kampo medicines are expected.
Animals↗
Effects of cacao liquor polyphenols on the susceptibility of low-density lipoprotein to oxidation in hypercholesterolemic rabbits.
The effects of cacao liquor polyphenols (CLP) on the susceptibility of low-density lipoprotein (LDL) to oxidation in hypercholesterolemic rabbits were examined. Six Japanese white rabbits which had been fed a high cholesterol diet (HCD) for 3 weeks were fed HCD containing 1% CLP for the following 10 days. The susceptibility of LDL to oxidation induced by 2-2'-azobis(4-methoxy-2, 4-dimethylvaleronitrile) (V-70) was evaluated by measuring the production of conjugated dienes and thiobarbituric acid reactive substances (TBARS). The lag time was significantly prolonged from 37.7 min before intake of CLP to 42.9, 44.2 and 45.8 min after 4, 7 and 10 days of CLP intake. TBARS production after intake of CLP was also markedly reduced compared with the level before intake. There was no difference in plasma lipid concentrations comparing the levels before and after CLP intake. In conclusion, in hypercholesterolemic rabbits, orally administered CLP was absorbed and distributed to the blood, and the resistance of LDL to oxidation was thereby increased.
Animals↗
Regulation of hepatic high density lipoprotein binding protein, HB2, expression after administration of simvastatin to rabbits.
HB2 a candidate HDL receptor, is quite distinct from other HDL receptors in its structure. However, while changes in cellular cholesterol content, or a reduction in cholesterol biosynthesis accompany corresponding changes in HB2 expression, the level at which these changes occur have not been determined and the regulation and the function of HB2 remain uncertain. In order to further investigate the regulation of HB2, we administered simvastatin to rabbits to reduce cholesterol biosynthesis and follow changes in HB2 mRNA in various tissues. Six rabbits were given 15 mg/kg of simvastatin by oral administration daily and another six rabbits were given the same volume of saline as a control, for 21 days. They were then sacrificed to obtain samples of blood, liver, lung, jejunum and brain. Simvastatin reduced plasma total cholesterol by 47% and free cholesterol concentrations in liver and lung by 25 and 10%, respectively. Northern blot analysis showed that simvastatin lowered the expression of HB2 significantly in the liver and lung by 54% and 42% respectively but not in the jejunum or brain. These results support the findings of a previous study showing that HDL binding activity of both HB1 and HB2, which was determined by ligand blotting using HDL3 as a ligand, were reduced after administering cholesterol lowering agents. (Arteriosclerosis, 10: 1045-1050,1990). The present study suggests that simvastatin down-regulated HB2 at the transcriptional stage. Although the complete physiological function of HB2 is unclear, it appears to play some role in the cholesterol metabolism, warranting further studies to elucidate the nature of this interaction.
Animals↗
Inhibition of low-density lipoprotein oxidation by astaxanthin.
Marine animals produce astaxanthin which is a carotenoid and antioxidant. In this study we determined the in vitro and ex vivo effects of astaxanthin on LDL oxidation. The oxidation of LDL was measured in a 1 ml reaction system consisting of increasing concentrations of astaxanthin (12.5, 25.0, 50.0 microg/ml), 400 microM V-70 (2, 2'-azobis(4-methoxy-2, 4-dimethylvaleronitrile)), and LDL (70 microg/ml protein). Astaxanthin dose, dependently significantly prolonged the oxidation lag time (31.5, 45.4, 65.0 min) compared with the control (19.9 min). For the ex vivo study 24 volunteers (mean age 28.2 [SD 7.8] years) consumed astaxanthin at doses of 1.8, 3.6,14.4 and 21.6 mg per day for 14 days. No other changes were made in the diet. Fasting venous blood samples were taken at days 0, +14. LDL lag time was longer (5.0, 26.2, 42.3 and 30.7% respectively) compared with day 0 after consuming astaxanthin at doses of 1.8, 3.6,14.4 and 21.6 mg for 14 days compared with day 0, but there was no difference in oxidation of LDL between day 0 (lag time 59.9+/-7.2 min) and day 14 (57.2+/-6.0 min) in the control group. Our results provide evidence that consumption of marine animals producing astaxanthin inhibits LDL oxidation and possibly therefore contributes to the prevention of atherosclerosis.
Adult↗
Binding of salicylhydroxamic acid and several aromatic donor molecules to Arthromyces ramosus peroxidase, investigated by X-ray crystallography, optical difference spectroscopy, NMR relaxation, molecular dynamics, and kinetics.
The X-ray crystal structure of the complex of salicylhydroxamic acid (SHA) with Arthromyces ramosus peroxidase (ARP) has been determined at 1.9 A resolution. The position of SHA in the active site of ARP is similar to that of the complex of benzhydroxamic acid (BHA) with ARP [Itakura, H., et al. (1997) FEBS Lett. 412, 107-110]. The aromatic ring of SHA binds to a hydrophobic region at the opening of the distal pocket, and the hydroxamic acid moiety forms hydrogen bonds with the His56, Arg52, and Pro154 residues but is not asscoiated with the heme iron. X-ray analyses of ARP-resorcinol and ARP-p-cresol complexes failed to identify the aromatic donor molecules, most likely due to the very low affinities of these aromatic donors for ARP. Therefore, we examined the locations of these and other aromatic donors on ARP by the molecular dynamics method and found that the benzene rings are trapped similarly by hydrophobic interactions with the Ala92, Pro156, Leu192, and Phe230 residues at the entrance of the heme pocket, but the dihedral angles between the benzene rings and the heme plane vary from donor to donor. The distances between the heme iron and protons of SHA and resorcinol are similar to those obtained by NMR relaxation. Although SHA and BHA are usually considered potent inhibitors for peroxidase, they were found to reduce compound I and compound II of ARP and horseradish peroxidase C in the same manner as p-cresol and resorcinol. The aforementioned spatial relationships of these aromatic donors to the heme iron in ARP are discussed with respect to the quantum chemical mechanism of electron transfer in peroxidase reactions.
Binding Sites↗
De novo expression of the class-A macrophage scavenger receptor conferring resistance to apoptosis in differentiated human THP-1 monocytic cells.
The class-A macrophage scavenger receptor (MSR) is a trimeric multifunctional protein expressed selectively in differentiated monomyeloid phagocytes which mediates uptake of chemically modified lipoproteins and bacterial products. This study investigated whether MSR plays a role in the regulation of apoptosis, a model of genetically programmed cell death. De novo expression of MSR occurred in human THP-1 monocytic cells differentiated with phorbol esters, which activated a nuclear transcription factor binding to the Ap1/ets-like domain of the MSR promoter. The phorbol ester-stimulated THP-1 cells also expressed increased levels of the pro-apoptotic gene products, caspase-3 and Fas ligand, but the cells exhibited no change in apoptosis. Global activation of GTP-binding proteins with fluoride anions triggered apoptosis of THP-1 cells in a time- and concentration-dependent manner, demonstrated by nuclear shrinkage and fragmentation and internucleosomal DNA fragmentation. However, the MSR-expressing THP-1 macrophage-like cells showed a significant reduction in apoptosis compared to undifferentiated control THP-1 cells, which produce MSR at undetectable levels. Fluoride stimulation also triggered apoptosis of human Jurkat T cells. Stimulation with phorbol ester made no difference in apoptosis between treated and untreated Jurkat cells. Finally, Chinese hamster ovary (CHO) cells overexpressing the class-A MSR type I by cDNA transfection showed markedly increased resistance to G-protein-coupled apoptosis. Thus, de novo expression of MSR associated with monocyte maturation into macrophages appears to confer the resistance of macrophages to apoptotic stimulation by G-protein activation.
Animals↗
Transcriptional inhibition by interleukin-6 of the class A macrophage scavenger receptor in macrophages derived from human peripheral monocytes and the THP-1 monocytic cell line.
Expression of the class A macrophage scavenger receptor (MSR) contributes to the uptake of modified low density lipoproteins (LDL) by macrophages and transformation of these cells into lipid-laden foam cells, which characterize atherosclerosis. Many environmental factors, in particular, proinflammatory cytokines and growth factors, can exert regulatory effects on MSR expression, whereas intracellular accumulation of cholesterol itself does not influence MSR levels to any considerable extent. In the present study, by using an in vitro model, we examined whether stimulation with interleukin-6 (IL-6), an immunoregulatory, multipotential cytokine, modulates the expression and activities of the MSR in macrophages. When treated with IL-6, macrophages derived from peripheral monocytes and phorbol 12-myristate 13-acetate (PMA)-differentiated THP-1 monocytic cells showed significantly reduced uptake and/or binding of the MSR ligand, acetylated LDL. This effect was paralleled by a reduction in the expression of MSR protein and mRNA. Analysis of MSR promoter activity in THP-1 cells transfected with an MSR promoter-reporter gene construct demonstrated decreased activity of the MSR promoter in IL-6-treated THP-1 macrophages. Electrophoretic mobility gel shift assay also showed a reduction in the binding of a transcription factor to the MSR promoter AP-1/ets elements in IL-6-treated cells. Thus, exposure to IL-6 may inhibit expression of the class A MSR in differentiated macrophages at transcriptional levels. This result suggests that this cytokine may modulate foam cell formation during atherogenesis.
Carbocyanines↗
[Lipoprotein and lipoprotein subfractions].
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Humans↗