Echinacea sanguinea and Echinacea pallida extracts stimulate glucuronidation and basolateral transfer of Bauer alkamides 8 and 10 and ketone 24 and inhibit P-glycoprotein transporter in Caco-2 cells.

The use of Echinacea as a medicinal herb is prominent in the United States, and many studies have assessed the effectiveness of Echinacea as an immunomodulator. We hypothesized that Bauer alkamides 8, 10, and 11 and ketone 24 were absorbed similarly either as pure compounds or from Echinacea sanguinea and Echinacea pallida ethanol extracts, and that these Echinacea extracts could inhibit the P-glycoprotein transporter in Caco-2 human intestinal epithelial cells. Using HPLC analysis, the permeation rate of Bauer alkamides by passive diffusion across Caco-2 cells corresponded with compound hydrophilicity (alkamide 8 > 10 > 11), independent of the plant extract matrix. Both Echinacea ethanol extracts stimulated apparent glucuronidation and basolateral efflux of glucuronides of alkamides 8 and 10 but not alkamide 11. Bauer ketone 24 was totally metabolized to more hydrophilic metabolites when administered as a single compound, but was also glucuronidated when present in Echinacea extracts. Bauer alkamides 8, 10, and 11 (175-230 µM) and ethanol extracts of E. sanguinea (1 mg/mL, containing ~ 90 µM total alkamides) and E. pallida (5 mg/mL, containing 285 µM total alkamides) decreased the efflux of the P-glycoprotein transporter probe calcein-AM from Caco-2 cells. These results suggest that other constituents in these Echinacea extracts facilitated the metabolism and efflux of alkamides and ketones, which might improve therapeutic benefits. Alkamides and Echinacea extracts might be useful in potentiating some chemotherapeutics, which are substrates for the P-glycoprotein transporter.

Glycemic index, insulinemic index, and satiety index of kefir.

OBJECTIVES: To determine glycemic, insulinemic, and satiety indices of 3 types of kefir. METHODS: This study was divided into 3 phases. In phase 1, 50 g of available carbohydrate from low-fat strawberry kefir or orange kefir was tested, and in phase 2, low-fat plain kefir containing 25 g of available carbohydrates was tested for glycemic index (GI), in both cases compared with an equivalent amount of glucose. In phase 3, 1000-kJ portions of all 3 types of kefirs were compared with white bread with the same energy content to determine the insulinemic index (II) and satiety index (SI) of all 3 kefirs. In all phases, a single-meal, randomized crossover design was performed in which the test meals were given to healthy adults, 5 men and 5 women. RESULTS: The total incremental plasma glucose area under the curve (iAUC) for strawberry, orange, and plain kefirs was significantly lower compared with the respective high-GI control food, which was glucose solution. However, the IIs and SIs of kefir did not differ significantly from the white bread. CONCLUSION: Kefir is a low- to moderate-GI food; however, its II was high. Although kefir had higher water content, the SI of kefir was not significantly different from white bread.

Artichoke extract lowered plasma cholesterol and increased fecal bile acids in Golden Syrian hamsters.

A study was conducted in hamsters to determine if artichoke leaf extract (ALE) could lower plasma total and non-HDL cholesterol by increasing fecal excretion of neutral bile acids and sterols. Sixty-four Golden Syrian hamsters (8 week old) were fed control diet or a similar diet containing ALE (4.5 g/kg diet) for 6 weeks. No significant changes for total cholesterol, HDL, non-HDL cholesterol triglycerides or fecal neutral sterols and bile acids were found after 21 days for ALE-fed animals compared with controls. But after 42 days, ALE-fed male hamsters had significantly lower total cholesterol (15%), non-HDL cholesterol (30%) and triglycerides (22%) and female hamsters fed ALE showed reductions of 15% for total cholesterol, 29% for non-HDL cholesterol and 29% for triglycerides compared with controls. Total neutral sterol and bile acids concentrations increased significantly by 50% and 53% in fecal samples of ALE fed males, and 82.4% and 25% in ALE fed females compared with controls. The ALE lowered hamster plasma cholesterol levels by a mechanism involving the greater excretion of fecal bile acids and neutral sterols after feeding for 42 days.

Bacteroides uniformis is a putative bacterial species associated with the degradation of the isoflavone genistein in human feces.

Inter-individual variation in isoflavone absorption depends on gut microbial degradation and affects the efficacy of these compounds. We hypothesized that inter-individual variation in fecal isoflavone disappearance coincided with variation in bacterial species. In vitro anaerobic fecal disappearance of isoflavones was measured from 33 participants by HPLC. Fecal microbial 16S rRNA variable region PCR products were obtained from 4 participants with the greatest and least genistein or glycitein degradation and were subjected to denaturing gradient gel electrophoresis. DNA bands with a homology of 90-95% to Bacteroides uniformis and Faecalibacterium prausnitzii were present in greater intensities in fecal samples showing a genistein disappearance rate constant of 1.47 ± 0.14 h(-1) compared with those with a genistein disappearance rate constant of 0.15 ± 0.03 h(-1) (P < 0.05). Human fecal bacterial species with DNA sequences 90-100% homologous to Tannerella forsythensis and 4 other species were present in greater intensities in fecal samples showing a glycitein disappearance rate constant of 0.57 ± 0.30 h(-1) compared with fecal samples with a glycitein disappearance rate constant of 0.08 ± 0.03 h(-1) (P < 0.05). In high degraders, B. uniformis may be a candidate for genistein degradation and T. forsythensis for glycitein degradation, based on fecal isoflavone degradation in the presence of these species. Bacteroides acidifaciens increased isoflavone disappearance in anaerobic human fecal incubations under nutrient-rich and -depleted conditions, suggesting this species as one responsible for the generally high degradation of isoflavones by humans. These fecal microbes are candidate biomarkers for interindividual variation in isoflavone uptake and efficacy.

Plasma caffeic acid is associated with statistical clustering of the anticolitic efficacy of caffeic acid in dextran sulfate sodium-treated mice.

We hypothesized that interindividual variability in the bioavailability of caffeic acid (CA) would influence its anticolitic efficacy and that mice may be appropriate for modeling human gut microbial metabolism of CA, which is thought to influence CA bioavailability. Anaerobic human fecal and mouse cecal sample mixtures were incubated with CA derivatives from Echinacea purpurea and compound disappearance rates were measured, which were similar in both sample types. CA metabolism, including formation of its main metabolite, m-hydroxyphenylpropionate, in the mouse cecum may usefully model human gut metabolism of this compound. Ten-week-old CD-1/IGS female mice were fed 120 mg CA/kg (n = 36) or control diet for 7 d (n = 12); one-half of each group then drank 1.25% dextran sulfate sodium (DSS) in water for 5 d. DSS-treated mice fed CA showed lessened colitic damage than did mice given DSS alone, with longer colons, greater body weight, and colonic Cyp4b1 expression. Cluster analysis of the cecal histopathological score showed that mice with severe cecal damage (mean cecal score = 8.5; n = 11) also had greater myeloperoxidase (MPO) activity and lower plasma CA compared with mice showing mild cecal damage (mean cecal score = 4.5; n = 4) (P < 0.05). Cecal score was positively correlated with colonic MPO activity (r = 0.72; P < 0.05) and negatively correlated with plasma CA (r = -0.57; P < 0.05). These studies indicated that the anticolitic efficacy of CA was related to variability in CA bioavailability, which may be influenced by gut microbial metabolism of this compound.

Increased CYP4B1 mRNA is associated with the inhibition of dextran sulfate sodium-induced colitis by caffeic acid in mice.

Susceptibility to inflammatory bowel diseases depends upon interactions between the genetics of the individual and induction of chronic mucosal inflammation. We hypothesized that administration of dietary phenolics, caffeic acid and rutin, would suppress upregulation of inflammatory markers and intestinal damage in a mouse model of colitis. Colitis was induced in C3H/ HeOuJ mice (8 weeks old, 6 male/6 female per treatment) with 1.25% dextran sulfate sodium (DSS) for 6 d in their drinking water. Rutin (1.0 mmol (524 mg)/kg in diet), caffeic acid (1.0 mmol (179 mg)/kg in diet), and hypoxoside extract (15 mg/d, an anticolitic phenolic control) were fed to the mice for 7 d before and during DSS treatment, as well as without DSS treatment. Body weight loss was prevented by rutin and caffeic acid during DSS treatment. Colon lengths in mice fed caffeic acid and hypoxoside during DSS treatment were similar to DSS-negative control. Food intake was improved and myeloperoxidase (MPO) was decreased with each phenolic treatment in DSS-treated mice compared with DSS treatment alone. Colonic mRNA expression of IL-17 and iNOS were inhibited when IL-4 was increased by each phenolic treatment combined with DSS, whereas CYP4B1 mRNA was increased only by caffeic acid in DSS-treated mice, compared with DSS treatment alone. Colonic and cecal histopathology scores of DSS-treated mice were significantly more severe (P < 0.01) than in mice fed caffeic acid before and during DSS treatment, based on mucosal height, necrosis, edema, erosion, and inflammatory cell infiltration. Although both rutin and caffeic acid suppressed the expression of selected inflammatory markers, only caffeic acid protected against DSS-induced colitis, in association with normalization of CYP4B1 expression. The inhibition of DSS-induced colitic pathology by caffeic acid was mediated by mechanisms in addition to anti-inflammatory effects that deserve further study.

Isoflavone glycitein diminished plasma cholesterol in female golden Syrian hamsters.

The soybean isoflavones, daidzein, genistein, and glycitein, were hypothesized to act as cholesterol-lowering components, separate from soy protein. Pure synthetic daidzein, genistein, or glycitein (0.9 mmol/kg diet) or a casein-based control diet was fed to groups of 10 female Golden Syrian hamsters for 4 weeks. Hamsters fed glycitein had significantly lower plasma total (by 15%) and non-HDL (by 24%) cholesterol compared with those fed casein (P<0.05). Daidzein and genistein's effects on these lipids did not differ from the effects of either casein or glycitein. Plasma HDL cholesterol and triglyceride concentrations were not significantly affected by dietary treatments. The percentage of urinary recovery of the ingested dose of each isoflavone was glycitein>daidzein>genistein (33.2%, 4.6%, 2.2%, respectively), with the apparent absorption of glycitein significantly greater than that of the other isoflavones. These data suggest that glycitein's greater cholesterol-lowering effect was due to its greater bioavailability, as reflected in its urinary recovery compared with that of the other isoflavones.

Synthesis and characterization of deoxynivalenol glucuronide: its comparative immunotoxicity with deoxynivalenol.

Deoxynivalenol (DON) is a mycotoxin commonly contaminating wheat, barley and corn. DON glucuronide (DONGLU) is a major DON metabolite. We synthesized and purified DONGLU and tested its immunotoxicity, hypothesizing that DONGLU would be much less toxic to K562 cells compared with DON. DONGLU was synthesized using rat liver microsomes, uridine-5'-diphosphoglucuronic acid and DON, and purified with a Sephadex LH-20 column and reverse phase HPLC. beta-Glucuronidase hydrolysis formed a product with retention time and UV spectrum identical with DON. Using atmospheric pressure chemical ionization in negative mode, the molecular mass (M-1) of purified DONGLU was 471 g/mol; in agreement with an expected molecular weight of 472 g/mol. MS and NMR indicated that the glucuronide moiety was conjugated with the carbon-3-hydroxyl group of DON. The cytotoxicity of DON and DONGLU were compared in cell culture using human erythroleukemia cell line K562. Fifty percent inhibition of cell number was observed with a DON concentration of 1.31 microM using a methylthaizol tetrazolium (MTS) cell viability assay whereas no significant cytotoxicity was observed for DONGLU at up to 270 microM. DONGLU did not influence DON toxicity at 0.5 microM, 1.3 microM and 8.4 microM concentration combinations of each compound. These data verified that DONGLU is a detoxification product of DON.

A controlled 2-mo dietary fat reduction and soy food supplementation study in postmenopausal women.

BACKGROUND: Low intake of dietary fat and high intake of soy foods have been suggested to partly explain the lower breast cancer rates in Asia, perhaps because of lower endogenous estrogens. OBJECTIVE: The objective was to assess the hormonal and nonhormonal effects of diets resembling an Asian diet in terms of total fat and soy food contents. DESIGN: Fifty-seven postmenopausal women participated in a randomized, controlled, dietary intervention study. The subjects consumed a very-low-fat diet (VLFD; 11% of energy as fat), a Step I diet (25% of energy as fat) supplemented with soy food (SFD; 50 mg isoflavones/d), or a control Step I diet (CD; 27% of energy as fat) with no soy food. All diets were prepared at the General Clinical Research Center of the University of Southern California. Serum hormones and other markers were measured at baseline and every 2 wk during the 8 wk of intervention. RESULTS: There were no significant differences in total estradiol and sex hormone binding globulin at the completion of the intervention between women in the SFD and VLFD groups and those in the CD group. Serum insulin decreased significantly in the SFD group, and leptin decreased significantly in the SFD and VLFD groups; however, these changes did not differ significantly from the changes in the CD group. CONCLUSIONS: This study does not provide evidence that ingestion of soy food or a VLFD significantly reduces estrogen concentrations in postmenopausal women. However, short-term changes in diet may have significant and beneficial effects on blood insulin and leptin concentrations.

Soyasaponins lowered plasma cholesterol and increased fecal bile acids in female golden Syrian hamsters.

A study was conducted in hamsters to determine if group B soyasaponins improve plasma cholesterol status by increasing the excretion of fecal bile acids and neutral sterols, to identify group B soyasaponin metabolites, and to investigate the relationship between a fecal group B soyasaponin metabolite and plasma lipids. Twenty female golden Syrian hamsters, 11-12 weeks old and 85-125 g, were randomly assigned to a control diet or a similar diet containing group B soyasaponins (containing no isoflavones), 2.2 mmol/kg, for 4 weeks. Hamsters fed group B soyasaponins had significantly lower plasma total cholesterol (by 20%), non-high-density lipoprotein (HDL) cholesterol (by 33%), and triglycerides (by 18%) compared with those fed casein (P < 0.05). The ratio of total cholesterol to HDL cholesterol was significantly lower (by 13%) in hamsters fed group B soyasaponins than in those fed casein (P < 0.05). The excretion of fecal bile acids and neutral sterols was significantly greater (by 105% and 85%, respectively) in soyasaponin-fed hamsters compared with those fed casein (P < 0.05). Compared with casein, group B soyasaponins lowered plasma total cholesterol levels and non-HDL cholesterol levels by a mechanism involving greater excretion of fecal bile acids and neutral sterols. Hamsters fed group B soyasaponins statistically clustered into two fecal soyasaponin metabolite-excretion phenotypes: high excreters (n = 3) and low excreters (n = 7). When high and low producers of this soyasaponin metabolite were compared for plasma cholesterol status, the high producers showed a significantly lower total-cholesterol-to-HDL-cholesterol ratio compared with the low producers (1.38 +/- 0.7 vs. 1.59 +/- 0.13; P < 0.03). Greater production of group B soyasaponin metabolite in hamsters was associated with better plasma cholesterol status, suggesting that gut microbial variation in soyasaponin metabolism may influence the health effects of group B soyasaponins.

Metabolism of glycitein (7,4'-dihydroxy-6-methoxy-isoflavone) by human gut microflora.

Gut microbial disappearance and metabolism of the soy isoflavone glycitein, 7,4'-dihydroxy-6-methoxyisoflavone, were investigated by incubating glycitein anaerobically with feces from 12 human subjects. The subjects' ages ranged from 24 to 53 years with a body mass index (BMI) of 20.9-25.8 kg/m(2) (mean BMI = 24.0 +/- 1.1 kg/m(2)). Glycitein disappearance followed an apparent first-order rate loss. Fecal glycitein disappearance rates for the subjects segregated into three different groups described as high (k = 0.67 +/- 0.14/h), moderate (k = 0.34 +/- 0.04/h), and low (k = 0.15 +/- 0.07/h) glycitein degraders (p < 0.0001). There was no dose effect on the disappearance rates for each subject from 10 to 250 microM glycitein (average k = 0.32 +/- 0.03/h, p > 0.05). Four putative glycitein metabolites, characterized by liquid chromatography-mass spectrometry (electrospray ionization using positive ionization mode), were dihydroglycitein, dihydro-6,7,4'-trihydroxyisoflavone, and 5'-O-methyl-O-desmethylangolensin. Two subjects produced a metabolite tentatively identified as 6-O-methyl-equol, and one subject produced daidzein as an additional metabolite of glycitein. These results show that glycitein is metabolized by human gut microorganisms and may follow metabolic pathways similar to other soy isoflavones.

Human gut microbial degradation of flavonoids: structure-function relationships.

The relationship between chemical structure and gut microbial degradation rates of 14 flavonoids, flavone, apigenin, chrysin, naringenin, kaempferol, genistein, daidzein, daidzin, puerarin, 7,4'-dihydroxyflavone, 6,4'-dihydroxyflavone, 5,4'-dihydroxyflavone, 5,3'-dihydroxyflavone, and 4'-hydroxyflavone, was investigated by anaerobically fermenting the flavonoids with human gut microflora (n = 11 subjects). Degradation rates for the 5,7,4'-trihydroxyl flavonoids, apigenin, genistein, naringenin, and kaempferol, were significantly faster than the other structural motifs. Puerarin was resistant to degradation by the gut microflora. Extensive degradation of flavonoids by gut microflora may result in lower overall bioavailability than those flavonoids that are slowly degraded because rapidly degrading flavonoids are less likely to be absorbed intact.

Fumonisin B-glucose reaction products are less toxic when fed to swine.

The effects of fumonisin B-glucose reaction products in swine diets was examined. Pigs were fed diets containing 528 micromol of total fumonisin B/kg (FB), 528 micromol of total FB-glucose adducts/kg (FB-G, 122 micromol of unreacted FB/kg), or 0 micromol of total FB/kg for 15 days to test the efficacy of the FB-G reaction products in detoxifying FB. Weight gain in FB pigs was lower than in FB-G or controls, which was correlated with feed intake reduction in FB pigs. Serum aspartate aminotransferase, gamma-glutamyltransferase, and total bilirubin in FB pigs were higher than in FB-G or control pigs. Serum sphinganine/shingosine ratios in FB pigs were higher than in FB-G or control pigs. Microscopic examination of tissues from FB pigs showed generalized liver necrosis and apoptosis with marked cellular pleomorphism and disorganized hepatic cords. The liver and kidneys in the FB-G group appeared to be normal. Tissues of controls were free of lesions. Results suggest that dietary FB-G products are less toxic to swine and may provide an detoxification approach in instances of widespread FB grain contamination (p < 0.05).

Soluble dietary fiber (Fibersol-2) decreased hunger and increased satiety hormones in humans when ingested with a meal.

We hypothesized that a digestion-resistant maltodextrin, Fibersol-2 (Archer Daniels Midland/Matsutani LLC, Decatur, IL, USA) may impact satiety by decreasing hunger, prolonging satiation, and/or increasing peripheral satiety signals. In a randomized, double-blind, placebo-controlled crossover study, healthy subjects (9 men and 10 women) underwent 3 treatments in which they consumed a standardized meal with a tea containing 0, 5, or 10 g of Fibersol-2. A visual analog scale questionnaire was given in 30-minute intervals to measure subjective appetite and satiety. Blood was drawn just before the meal (time 0) and at 30, 60, 90, 120, 180, and 240 minutes after meal for measurements of plasma ghrelin, cholecystokinin, gastrin, peptide YY, gastric inhibitory polypeptide, and glucagon-like peptide-1, all by enzyme-linked immunosorbent assay. There were significant delays in hunger and increased satiety for 1.5 to 2 hours after treatment with 10 g of Fibersol-2. These delays did not occur after ingesting 0 or 5 g Fibersol-2 at any time. Control and 5 g Fibersol-2 treatments did not suppress increases in hunger postmeal; hunger scores increased and satiety scores decreased significantly (P < .05) at all time points relative to the first postmeal assessment. Plasma peptide YY and glucagon-like peptide-1 were significantly increased by the ingestion of meal with tea containing 10 g Fibersol-2 compared with 0 or 5 g Fibersol-2 (P < .05). This study demonstrated that 10 g Fibersol-2 with a meal stimulated production of satiety hormones and enhanced satiety.

Increased Butyrate Production During Long-Term Fermentation of In Vitro-Digested High Amylose Cornstarch Residues with Human Feces.

An in vitro semi-continuous long-term (3 wk) anaerobic incubation system simulating lower gut fermentation was used to determine variability in gut microbial metabolism between 4 predigested high amylose-resistant starch residues (SR): SRV, SRVI, SRVII, and SRGEMS in human fecal samples. Subjects participated twice, 5 mo apart: 30 in Phase I (15 lean, 9 overweight and 6 obese), 29 in Phase II (15 lean, 9 overweight, 5 obese); 13 of 15 lean subjects participated in both phases. Of the 4 SRs, SRV displayed the highest gelatinization temperature, peak temperature, enthalpy changes, and the least digestibility compared with the other SRs. In both phases, compared with blank controls, all SRs increased butyrate ∼2-fold which stabilized at week 2 and only SRV caused greater propionate concentration (∼30%) after 3 wk which might have been partly mediated by its lesser digestibility. Fecal samples from lean and overweight/obese subjects incubated with SRs showed similar short-chain fatty acid production across both time points, which suggests that resistant starch may benefit individuals across BMIs.

Soy protein with or without isoflavones, soy germ and soy germ extract, and daidzein lessen plasma cholesterol levels in golden Syrian hamsters.

Dietary isolated soy protein (ISP, containing approximately equal amounts of daidzein and genistein), ethanol-extracted ISP (ISP (-)), soygerm or soygerm extract (containing large amounts of daidzein and glycitein and little genistein) and the isoflavone, daidzein, were hypothesized to lessen plasma cholesterol in comparison with casein. Sixty male and 60 female golden Syrian hamsters (6-8 weeks of age) were randomly assigned to six treatments fed for 10 weeks. Four of the experimental diets (ISP, daidzein, soygerm, and soygerm extract) contained 1.3 mmol total isoflavones/kg. The ISP (-) diet contained 0.013 mmol isoflavone/kg, whereas the casein diet contained no isoflavones. Hamsters fed ISP, ISP (-), daidzein, soygerm, and soygerm extract had significantly less plasma total cholesterol (by 16%-28%), less non-HDL cholesterol (by 15%-50%) and less non-HDL/HDL cholesterol ratios compared with hamsters fed casein (P < 0.01). For male hamsters, there were no differences among treatments in plasma HDL concentrations. Female hamsters fed ISP (-) had significantly greater HDL levels (P < 0.01) than females fed casein or daidzein. Triglyceride concentration was significantly less in hamsters fed ISP (-) compared with the casein-fed females. Because soy protein with or without isoflavones, soygerm and soygerm extract, and daidzein lessened plasma cholesterol to an approximately equal extent, soy protein alone, varying mixtures of isoflavones, and other extractable components of soy are responsible for cholesterol-lessening effects of soy foods, mainly due to their effects to lessen LDL cholesterol.

Bioavailability of isoflavones.

Isoflavones are disease protective components of soybeans. Isoflavone metabolism and bioavailability are key to understanding their biological effects. Isoflavone glucuronides, dominant biotransformation products in humans that are more hydrophilic than isoflavone aglycones, activate human natural killer cells in vitro but are less toxic to NK cells than the parent aglycones. Gut microbial isoflavone metabolites have also been identified, but remain to be well characterized. Gut transit time (GTT) seems to be a significant determinant of isoflavone bioavailability because women with more rapid GTT (<40 h) experienced 2-3-fold greater absorption of isoflavones than did women with longer GTT (>65 h). Isoflavone metabolism varies a great deal among individuals, thus limiting the quantitative value of urine or plasma isoflavones as biomarkers of soy ingestion. Defining and lessening interindividual variation in isoflavone bioavailability, and characterizing health-related effects of key isoflavone metabolites are likely to be crucial to further understanding of the health benefits of isoflavones.

Quantification of the group B soyasaponins by high-performance liquid chromatography.

High-performance liquid chromatographic methods were developed for the isolation and quantitative determination of the group B soyasaponins, including 2,3-dihydro-2,5-dihydroxy-6-methyl-4H-pyran-4-one (DDMP)-conjugated soyasaponins alphag, betag, and betaa, and their non-DDMP counterparts, soyasaponins V, I, and II, respectively, with formononetin used as the internal standard. The limits of quantification for soy products were 0.11-4.86 micromol/g. The within-day and between-days assay coefficients of variation were <9.8 and < 14.3%, respectively. The group B soyasaponin concentrations in 46 soybean varieties ranged from 2.50 to 5.85 micromol/g. Soy ingredients (soybean flour, toasted soy hypocotyls, soy protein isolates, textured vegetable protein, soy protein concentrates, and Novasoy) and soy foods (commercial soy milk, tofu, and tempeh) contained the group B soyasaponins from 0.20 to 114.02 micromol/g. There was no apparent correlation between isoflavone and soyasaponin concentrations in the soy products examined.

Human fecal metabolism of soyasaponin I.

The metabolism of soyasaponin I (3-O-[alpha-L-rhamnopyranosyl-beta-D-galactopyranosyl-beta-D-glucuronopyranosyl]olean-12-ene-3beta,22beta,24-triol) by human fecal microorganisms was investigated. Fresh feces were collected from 15 healthy women and incubated anaerobically with 10 mmol soyasaponin I/g feces at 37 degrees C for 48 h. The disappearance of soyasaponin I in this in vitro fermentation system displayed apparent first-order rate loss kinetics. Two distinct soyasaponin I degradation phenotypes were observed among the subjects: rapid soyasaponin degraders with a rate constant k = 0.24 +/- 0.04 h(-)(1) and slow degraders with a k = 0.07 +/- 0.02 h(-)(1). There were no significant differences in the body mass index, fecal moisture, gut transit time, and soy consumption frequency between the two soyasaponin degradation phenotypes. Two primary gut microbial metabolites of soyasaponin I were identified as soyasaponin III (3-O-[beta-D-galactopyranosyl-beta-D-glucuronopyranosyl]olean-12-ene-3beta,22beta,24-triol) and soyasapogenol B (olean-12-ene-3beta,22beta,24-triol) by NMR and electrospray ionized mass spectroscopy. Soyasaponin III appeared within the first 24 h and disappeared by 48 h. Soyasapogenol B seemed to be the final metabolic product during the 48 h anaerobic incubation. These results indicate that dietary soyasaponins can be metabolized by human gut microorganisms. The sugar moieties of soyasaponins seem to be hydrolyzed sequentially to yield smaller and more hydrophobic metabolites.

Characterization of fumonisin B(1)-glucose reaction kinetics and products.

The reaction of fumonisin B(1) with the reducing sugar D-glucose can block the primary amine group of fumonisin B(1) and may detoxify this mycotoxin. A method to separate hundred milligram quantities of fumonisin B(1)-glucose reaction products from the excess D-glucose with a reversed-phase C(18) cartridge was developed. Mass spectrometry revealed that there were four primary products in this chain reaction when fumonisin B(1) was heated with D-glucose at 65 degrees C for 48 h: N-methyl-fumonisin B(1), N-carboxymethyl-fumonisin B(1), N-(3-hydroxyacetonyl)-fumonisin B(1), and N-(2-hydroxy, 2-carboxyethyl)-fumonisin B(1). The N-(1-deoxy-D-fructos-1-yl) fumonisin B(1) (fumonisin B(1)-glucose Schiff's base) was detected by mass spectrometry when fumonisin B(1) was heated with D-glucose at 60 degrees C. The nonenzymatic browning reaction of fumonisin B(1) with excess D-glucose followed apparent first-order kinetics. The activation energy, E(a), was 105.7 kJ/mol. Fumonisin B(1) in contaminated corn could precipitate the nonenzymatic browning reaction with 0.1 M D-glucose at 60 and 80 degrees C.