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1 eospecificity of the bacterial production of equol.
2 lity to produce and excrete large amounts of equol.
3 ned for their ability to convert daidzein to equol.
4 diet, particularly, daidzein, genistein, and equol.
5  be recapitulated by the daidzein metabolite equol.
6                     Eight profiles contained equol.
7 dependent protein synthesis was increased by equol.
8 ual differences in conversion of daidzein to equol.
9  phytoestrogens, genistein and daidzein, and equol (a daidzein metabolite produced by intestinal micr
10                  We previously reported that equol, a metabolite of the soy isoflavone daidzein, may
11 o the potential cardioprotective benefits of equol, a microbial-derived metabolite of the isoflavone
12 ch soy isoflavones (genistein, daidzein, and equol) afford protection against oxidative stress in CVD
13                                              Equol also increased metastatic cancer cell viability.
14 0-50% have the bacteria capable of producing equol and 80-90% harbor O-desmethylangolensin-producing
15                    Plasma and urinary [13C]R-equol and [13C]S-equol concentrations were measured by t
16 microbial metabolism in animal food sources (equol and enterolactone).
17 molecular basis for the anticancer action of equol and may partially account for the reported chemopr
18 er the intervention or in BMD change between equol and non-equol producers.
19 ra activities [beta-glucoside hydrolysis and equol and O-desmethylangolensin (O-DMA) production].
20                                              Equol and O-desmethylangolensin (ODMA) are products of g
21 he soy isoflavone daidzein is metabolized to equol and O-desmethylangolensin (ODMA) by intestinal bac
22 ctors that influence the capacity to produce equol and O-desmethylangolensin are not clearly establis
23  biochanin-A and their mammalian metabolites equol and O-desmethylangolensin in human plasma, urine,
24 es produced by human intestinal bacteria are equol and O-desmethylangolensin.
25 men had detectable concentrations of urinary equol and ODMA (>87.5 ng/mL), respectively, and were cla
26                                              Equol and ODMA producers reported higher overall physica
27 ons of daidzein intake and gut metabolism to equol and of equol intake from animal products in low-so
28 ced by low or undetectable concentrations of equol and other metabolites, and is maintained by consta
29  was to compare the pharmacokinetics of S-(-)equol and R-(+)equol by using [13C] stable-isotope-label
30 rogen equol occurs as diastereoisomers, S-(-)equol and R-(+)equol, both of which have significant bio
31 abolished by diarylpropionitrile, genistein, equol, and bisphenol A, whereas its coactivation at the
32 ned the interactions of genistein, daidzein, equol, and liquiritigenin with estrogen receptors ERalph
33 ers and mean quantities of dihydrogenistein, equol, and O-desmethylangolensin in the urine of ileosto
34  for isoflavonoids (ie, daidzein, genistein, equol, and O-desmethylangolensin) and lignans (enterodio
35  cell viability and mammosphere formation by equol, and results in a significant down-regulation of e
36 l half-lives for biochanin A, genistein, and equol are expected to vary on the basis of pH as well as
37 e activities of daidzein and its metabolite, equol, are not understood.
38 mers, despite current interest in developing equol as a nutraceutical or pharmaceutical agent.
39         Our studies definitively establish S-equol as the exclusive product of human intestinal bacte
40 urs as diastereoisomers, S-(-)equol and R-(+)equol, both of which have significant biological actions
41 or c-Jun N-terminal kinase, was inhibited by equol but not by daidzein.
42 plastic cell transformation was inhibited by equol, but not daidzein, at noncytotoxic concentrations
43                                    In vitro, equol, but not daidzein, up-regulated eIF4G without affe
44  the pharmacokinetics of S-(-)equol and R-(+)equol by using [13C] stable-isotope-labeled tracers to f
45  alpha was decreased in animals treated with equol compared to those treated with 17beta-estradiol.
46                                  Plasma [13C]equol concentration appearance and disappearance curves
47 ich was significantly associated with plasma equol concentrations (R = -0.36, P = 0.01).
48 nverse association between urinary and serum equol concentrations and breast and prostate cancer risk
49              These results also suggest that equol concentrations in low-soy-consuming populations ma
50  was observed in non-EPs despite mean plasma equol concentrations reaching 3.2 mumol/L.
51   Plasma and urinary [13C]R-equol and [13C]S-equol concentrations were measured by tandem mass spectr
52 cursor daidzein contributed to the increased equol concentrations.
53 umes, were significant correlates of urinary equol concentrations; milk products were more strongly c
54 of ingested daidzin was excreted in urine as equol conjugate in one man and one woman after the first
55                  Biochanin A, genistein, and equol degraded relatively slowly by direct photolysis at
56 o and ex vivo pull-down assays revealed that equol directly bound with glutathione S-transferase-MEK1
57                                              Equol does not affect glycitein bioavailability.
58                                              Equol dose-dependently attenuated TPA-induced activation
59                                              Equol dose-dependently inhibited neoplastic transformati
60 f both enantiomers, and the affinity of each equol enantiomer for estrogen receptors was measured.
61 re of equol, to examine whether the S- and R-equol enantiomers are bioavailable, and to ascertain whe
62 nsuming both diets could convert daidzein to equol ex vivo.
63                        The amount of urinary equol excreted did not relate to the changes in blood li
64 mpare urinary isoflavonoid excretion between equol excreters and nonexcreters.
65 , which did not differ significantly between equol excreters and nonexcreters.
66 f the subjects were identified previously as equol excreters and the other half as equol nonexcreters
67                   These results suggest that equol excretion may be related to the fermentable carboh
68                                    In women, equol excretion was associated with higher intake of die
69 ot differ between subjects with high and low equol excretion.
70                           Dietary sources of equol from animal products have been identified, which h
71 may not reflect the endogenous production of equol from the microbial metabolism of daidzein-an obser
72 uired an ability to exclusively synthesize S-equol from the precursor soy isoflavone daidzein, and it
73 conjugates (daidzein, O-desmethylangolensin, equol, genistein, and glycitein) and two lignans (entero
74 soflavones (daidzein, O-desmethylangolensin, equol, genistein, and glycitein) and two lignans (entero
75         In vitro kinase assays revealed that equol greatly inhibited MEK1, but not Raf1, kinase activ
76 ened subjects (30 men and 30 women) excreted equol (>2000 nmol/d).
77 ever, a single dose of commercially produced equol had no cardiovascular benefits in non-EPs.
78                                            S-equol has a high affinity for estrogen receptor beta (K(
79                             The discovery of equol in human urine more than 2 decades ago and the fin
80 itical in unlocking the vascular benefits of equol in men, and long-term trials should focus on confi
81 tents of daidzein, glycitein, genistein, and equol in milk as well as fresh and mature yogurts was es
82                                    Moreover, equol increased the polysomal association of mRNAs for p
83 gative (ER-) metastatic breast cancer cells, equol induced elevated levels of eIF4G, which were assoc
84                          Here we report that equol inhibits 12-O-tetradecanoylphorbol-13-acetate (TPA
85 in intake and gut metabolism to equol and of equol intake from animal products in low-soy-consuming p
86 in low-soy-consuming populations may reflect equol intakes from mammalian milk sources and may not re
87 tinal microflora) are antioxidants in vitro; equol is a particularly good inhibitor of LDL oxidation
88 ested that the antitumor-promoting effect of equol is due to the inhibition of cell transformation ma
89 eceptor beta (K(i) = 0.73 nmol/L), whereas R-equol is relatively inactive.
90         Therefore, up-regulation of eIF4G by equol may result in increased translation of pro-cancer
91  genistein, total isoflavonoids (TIFLs), and equol (measured by HPLC/photodiode array/mass spectromet
92 Knockdown of eIF4GI also markedly reduces an equol-mediated increase in IRES-dependent mRNA translati
93 sly as equol excreters and the other half as equol nonexcreters.
94 holesterol concentrations than those seen in equol nonproducers.
95 atment period was analyzed for isoflavonoid (equol, O-desmethylangolensin, genistein, and daidzein) a
96                    The nonsteroidal estrogen equol occurs as diastereoisomers, S-(-)equol and R-(+)eq
97 ve compounds, namely genistein, daidzein and equol, on the inflammatory responses induced by lipopoly
98 ]equol were higher than those of S-(-)[2-13C]equol or the racemate.
99                                  Estrone and equol persisted along the waste disposal route.
100 a support favorable associations between the equol producer (EP) phenotype and cardiometabolic health
101 xyestrone (16alpha-OH) ratio (P < 0.05), and equol-producer status (P < 0.05) compared with CON.
102 ypes and oppositely regulated expression for equol producers (down) and nonproducers (up) after HG su
103                                              Equol producers (n = 17) had larger reductions in diasto
104             The separation of the group into equol producers (n = 30) and nonproducers (n = 55) showe
105 s, respectively; P < 0.01) compared with non-equol producers (n = 30).
106 data analysis was performed per substudy for equol producers and nonproducers separately.
107  (P = 0.5) in bone calcium retention between equol producers and nonproducers.
108 educed serum LDL cholesterol equally in both equol producers and nonproducers.
109 nflammation-related genes was upregulated in equol producers but downregulated in nonproducers, indep
110 L cholesterol and apolipoprotein A-I only in equol producers compared with reductions in nonproducers
111                  Compared with nonproducers, equol producers were more likely (P < or = 0.05) to be H
112 vements in arterial stiffness were observed; equol producers were particularly responsive.
113                                  However, in equol producers, ~35% of our study population, soy consu
114 induced anti-inflammatory gene expression in equol producers.
115 ntion or in BMD change between equol and non-equol producers.
116 t of isoflavones in a soy supplement and the equol-producing ability of the individual on postmenopau
117  specific isoflavone content or the variable equol-producing capacity of individuals.
118 ore effective in maintaining bone density in equol-producing individuals.
119              Participants were randomized by equol-producing phenotype, and data analysis was perform
120 ere influenced by supplement composition and equol-producing phenotype, whereas estrogen-responsive e
121 es after LG supplementation (n = 24) in both equol-producing phenotypes and oppositely regulated expr
122  in postmenopausal women regardless of their equol-producing status, and mixed isoflavones in their n
123             We observed associations between equol production and ethnicity, education, constipation,
124 ng studies: a large cross-sectional study of equol production in humans with a soy challenge, a compa
125 te profile (2-OH:16alpha-OH), and stimulated equol production in postmenopausal women with osteopenia
126 in receptor (Gln223Arg)] and with respect to equol production were investigated.
127 lesteryl ester transfer protein (TaqIB)] and equol production were investigated.
128 ones were observed according to subgroups of equol production.
129  estrone, androstenedione, progesterone, and equol remained detectable in soil at 2 months postapplic
130                                              Equol specifically increased the protein expression of I
131 e objective of the study was to show whether equol status determines the effectiveness of soy foods t
132  ex vivo kinase assay also demonstrated that equol suppressed TPA-induced MEK1 kinase activity in JB6
133 availability, and suggests that low doses of equol taken twice daily may be sufficient to achieve bio
134                                         S-(-)equol, the naturally occurring enantiomer produced by 20
135 idzein, and it is significant that, unlike R-equol, this enantiomer has a relatively high affinity fo
136 fect of providing commercially produced S-(-)equol to non-EPs.
137 assessed the ability of 17beta-estradiol and equol to regulate markers of hippocampal bioenergetic ca
138  were to characterize the exact structure of equol, to examine whether the S- and R-equol enantiomers
139              Similarly, 17beta-estradiol and equol treatment had no effect on mitochondrial fission a
140 ficant effects of either 17beta-estradiol or equol treatment on glycolytic protein expression in the
141 mRNAs that are translationally stimulated by equol treatment.
142                                              Equol, unlike the soy isoflavones daidzein or genistein,
143 regulator of the cancer-promoting effects of equol via up-regulation of eIF4GI and selective initiati
144                    The isoflavone metabolite equol was by far the predominant phytoestrogen species,
145 esponses with the ERbeta-preferring molecule equol was consistent with overall nonresponsiveness.
146  of chiral-phase HPLC and mass spectrometry, equol was isolated from human urine and plasma, and its
147            The elevated eIF4G in response to equol was not associated with eIF4E or 4E-binding protei
148 ly, no benefit of commercially produced S-(-)equol was observed in non-EPs despite mean plasma equol
149 ong those mRNAs translationally increased by equol was the oncogene and eIF4G enhancer, c-Myc.
150 on rates (k(e)) for genistein, daidzein, and equol were 0.1, 0.16, and 0.08 h(-1), respectively, in w
151 es of conjugates of genistein, daidzein, and equol were 24%, 66%, and 28% of the amounts ingested in
152            The pharmacokinetics of S- and R- equol were determined in 3 healthy adults after single-b
153  The pharmacokinetics of racemic (+/-)[2-13C]equol were different from those of the individual enanti
154 ity and fractional absorption of R-(+)[2-13C]equol were higher than those of S-(-)[2-13C]equol or the
155 , the amounts of daidzein and its metabolite equol were significantly higher in samples obtained from
156 n, formononetin, biochanin A, genistein, and equol were studied under simulated solar light and natur
157 turation, the concentrations of daidzein and equol were unaffected, while the glycitein concentration
158 in, and the intestinally derived metabolite, equol, were compared in 4-month-old infants fed exclusiv
159 rate assessment, non-EPs consumed 40 mg S-(-)equol with identical vascular measurements performed 2 h

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