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The identification (by gas chromatography-mass spectrometry and n.m.r.) for the first time of the weak oestrogen equol [7-hydroxy-3-(4'-hydroxyphenyl)chroman] in human urine is described. Preliminary results of its quantitative excretion in urine are reported and the potential significance of the occurrence of this compound is discussed.
BACKGROUND: The hypocholesterolemic effects of soy foods are well established, and it has been suggested that isoflavones are responsible for this effect. However, beneficial effects of isolated isoflavones on lipid biomarkers of cardiovascular disease risk have not yet been shown. OBJECTIVE: The objective was to investigate the effects of isolated soy isoflavones on metabolic biomarkers of cardiovascular disease risk, including plasma total, HDL, and LDL cholesterol; triacylglycerols; lipoprotein(a); the percentage of small dense LDL; glucose; nonesterified fatty acids; insulin; and the homeostasis model assessment of insulin resistance. Differences with respect to single nucleotide polymorphisms in selected genes [ie, estrogen receptor alpha (XbaI and PvuII), estrogen receptor beta (AluI), and estrogen receptor beta(cx) (Tsp509I), endothelial nitric oxide synthase (Glu298Asp), apolipoprotein E (Apo E2, E3, and E4), cholesteryl ester transfer protein (TaqIB), and leptin receptor (Gln223Arg)] and with respect to equol production were investigated. DESIGN: Healthy postmenopausal women (n = 117) participated in a randomized, double-blind, placebo-controlled, crossover dietary intervention trial. Isoflavone-enriched (genistein-to-daidzein ratio of 2:1; 50 mg/d) or placebo cereal bars were consumed for 8 wk, with a wash-out period of 8 wk before the crossover. RESULTS: Isoflavones did not have a significant beneficial effect on plasma concentrations of lipids, glucose, or insulin. A significant difference between the responses of HDL cholesterol to isoflavones and to placebo was found with estrogen receptor beta(cx) Tsp509I genotype AA, but not GG or GA. CONCLUSIONS: Isoflavone supplementation, when provided in the form and dose used in this study, had no effect on lipid or other metabolic biomarkers of cardiovascular disease risk in postmenopausal women but may increase HDL cholesterol in an estrogen receptor beta gene-polymorphic subgroup.
Fructooligosaccharides (FOS) stimulate the growth of bifidobacteria, which cleave isoflavone conjugates to yield the corresponding aglycones and metabolites. In a previous study, FOS modified the absorption and enterohepatic recirculation of isoflavones in rats. In the present study, we determined the effect of the combination of dietary FOS and isoflavone conjugates on bone mass in ovariectomized (OVX) and surgical control mice. After undergoing OVX or sham operation, female ddY mice (8 wk old, n = 64) were randomly assigned to four groups: a purified control diet (AIN-93G) group, a FOS diet (AIN-93G + 5% FOS) group, an isoflavone diet (AIN-93G + 0.2% isoflavone conjugates) group, or a FOS and isoflavone diet (AIN-93G + 5% FOS + 0.2% isoflavone conjugates) group. After 6 wk, the mice were killed and the blood and femora were sampled immediately. In OVX mice, both isoflavone conjugates and FOS prevented femoral bone loss. An additive effect of dietary isoflavone conjugates and FOS was observed by dual-energy X-ray absorptiometry in the distal part of the femur and in trabecular bone, by peripheral quantitative computed tomography. Moreover, FOS increased cecal beta-glucosidase activity and equol production from daidzein in both OVX and surgical control mice fed isoflavone conjugates. These results suggest that FOS increase the bioavailability of isoflavones, leading to cooperative effects in the prevention of osteopenia in OVX mice.
Extrarenal synthesis of the active vitamin D metabolite 1,25-dihydroxyvitamin-D3 (1,25-D) has been observed in cells derived from human organs prone to sporadic cancer incidence. Enhancement of the synthesizing hydroxylase CYP27B1 and reduction of the catabolic CYP24 could support local accumulation of the antimitotic steroid, thus preventing formation of tumors of e.g., colon and breast. By applying quantitative RT-PCR and HPLC it was observed that in colon-(Caco-2) and breast-(MCF-7) derived cells, 17beta-estradiol and genistein induced CYP27B1 but reduced CYP24 activity, while equol was inactive. Mammary cells express both estrogen receptors (ER) a and beta, while colon cells express mainly ERbeta, possibly explaining why MCF-7 cells were more affected. These results indicate a potential, new approach for cancer prevention by counteraction of the 1,25-D-driven negative feedback, i.e., down-regulation of CYP27B1 and up-regulation of CYP24, which prevents its own local accumulation. However, mammary cells may be more susceptible to this than colonocytes.
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Equol and O-desmethylangolensin (O-DMA) are products of bacterial metabolism of daidzein, an isoflavone in soybeans; thus, the presence or absence of equol and/or O-DMA in urine is a marker of particular intestinal bacteria profiles. Plasma hormone concentrations may be lower in pre-menopausal women who harbor the bacteria capable of producing equol (equol producers) compared to women who do not (equol non-producers). We evaluated concentrations of serum hormones, sex hormone-binding globulin (SHBG), and urinary 2-hydroxyestrone (2-OH E(1)) and 16alpha-hydroxyestrone (16alpha-OH E(1)) in relation to equol-producer and O-DMA-producer phenotypes in 89 post-menopausal women. Follicle stimulating hormone (FSH) was 23% greater in O-DMA-producers compared to non-producers (P = 0.04). No significant differences in serum estrogens, androgens, metabolic hormones, or SHBG were observed in relation to either daidzein-metabolizing phenotype. Compared with non-producers within each phenotype, age-adjusted 2-OH E(1):16alpha-OH E(1) was 27% greater (P = 0.06) in equol-producers and 9% greater (P > 0.10) in O-DMA-producers, and 2-OH E(1) concentrations were 24% greater in equol producers (P = 0.07) and 42% greater in O-DMA producers (P = 0.02). No significant differences in 16alpha-OH E(1) were observed in relation to either phenotype. These results suggest that interindividual variability in intestinal bacteria may be related to differences in products of hormone metabolism in post-menopausal women.
OBJECTIVE: The aim of this study was to determine whether equol excretion status and plasma hormone and leptin concentrations can be influenced by consumption of a probiotic supplement. A secondary focus was to investigate whether male equol excretors have a hormone profile consistent with reduced prostate cancer risk. DESIGN: The design was a randomized, single-blinded, placebo-controlled, parallel-arm trial. SUBJECTS: Thirty-one (31) of the initially enrolled 39 subjects, 18 to 37 years old, completed all study requirements. INTERVENTION: Subjects consumed either probiotic capsules (containing Lactobacillus acidophilus and Bifidobacterium longum) or placebo capsules for 2 months. Fasting plasma concentrations of testosterone (T), dihydrotestosterone (DHT), androstanediol glucuronide (AAG), androstenedione (A), dehydroepiandrosterone sulfate (DHEAS), sex hormone-binding globulin (SHBG), and leptin were measured on days 1 and 57. Urinary excretion of genistein, glycitein, daidzein, O-desmethylangolensin (O-Dma), and equol was measured on days 4 and 61 following a 4-day soy challenge. RESULTS: Probiotic consumption did not significantly alter equol excretor status, plasma hormone, or leptin concentrations in these subjects. At baseline, there were no differences in plasma hormone concentrations between equol excretors and nonexcretors; however, the low number of equol excretors included in this study limits the strength of this finding. CONCLUSIONS: The 2-month intervention with probiotic capsules did not significantly alter equol excretion, plasma hormone, or leptin concentrations in these subjects. A secondary finding was that male equol excretors in this study did not exhibit a hormone profile consistent with reduced prostate cancer risk, although this result should be interpreted with caution.
OBJECTIVES: Intestinal bacterial metabolize the soy isoflavone daidzein to O-desmethylangolensin (O-DMA) or equol. Some individuals do not excrete O-DMA or equol after soy consumption, suggesting they do not harbor bacteria capable of producing these metabolites. The aim of this study was to evaluate bone mineral density (BMD) in relation to presence of these urinary metabolites. METHODS: BMD, determined by whole-body dual X-ray absorptiometry scan, was age-adjusted and evaluated in relation to O-DMA-producer and equol-producer phenotypes in 92 postmenopausal women, aged 50-75 years. Women consumed supplemental soy foods (daidzein source) for 3 days and collected a first-void urine sample on the fourth day in order to determine metabolic phenotypes. RESULTS: In O-DMA producers (n=76) compared to O-DMA non-producers (n=16), greater total, leg and head BMD (p<0.05) were observed. Total BMD among the O-DMA producers (geometric mean=1.04 g/cm2) was 6% greater than total BMD among the O-DMA non-producers (geometric mean=0.98 g/cm2). Total and site-specific BMD did not differ between equol producers (n=24) and non-producers (n=68) (p>0.05). In exploratory analyses, among regular soy consumers, spinal BMD was 20% lower among the equol producers than non-producers, whereas, among soy non-consumers, no such difference was observed (p-interaction<0.05). Among equol producers, circulating estrone and free estradiol concentrations were inversely or not associated with total BMD, whereas, among equol non-producers, these hormones were positively associated (p-interaction<0.05). CONCLUSIONS: Our results provide evidence that intestinal bacterial composition may influence BMD in postmenopausal women. Further studies characterizing associations of intestinal bacterial profiles with BMD are warranted.
We have investigated the metabolism of isoflavones and lignans in germ-free (GF) rats and rats associated with human faecal bacteria (human flora associated [HFA] rats), in order to provide unequivocal evidence for the role of the gut microflora in the absorption and metabolism of these phytoestrogens. Furthermore, we have investigated whether certain metabolic characteristics (high equol-producing and low equol-producing status) of human intestinal floras can be transferred to GF rats. Germ-free rats fed a soy-isoflavone containing diet excreted large quantities of daidzein and genistein in urine indicating that the gut microflora is not required for the absorption of isoflavones. The isoflavone metabolites equol, O-desmethylangolensin and the lignan enterolactone were not detectable in urine from the GF rats, but were present in HFA rat urine, indicating that they were products of gut microflora activity. Colonization of GF rats with a faecal flora from a human subject with the capacity to convert daidzein to equol, resulted in the rats excreting substantial amounts of the metabolite. In contrast, equol was undetectable in urine of HFA rats associated with a faecal flora from a low equol-producing subject. The results therefore show that the inability of some subjects to produce equol is a consequence of the lack of specific components of the gut microflora.