![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
Department of Gastrointestinal Microbiology, German Institute of Human Nutrition (DIfE), 14558 Nuthetal, Germany
* To whom correspondence should be addressed. E-mail: blaut{at}mail.dife.de.
 |
ABSTRACT |
|---|
 TOP ABSTRACT LITERATURE CITED |
|---|
Phylogenetic diversity and metabolic diversity
Recent evidence indicates that the cultivable fecal bacteria represent only a fraction of the bacteria actually present in the gut. The application of culture-independent methods revealed that the diversity of the fecal gut microbiota is considerably higher than anticipated (1,2). The proportion of undescribed species varied from 30 to 90%. Some 16S rRNA sequences indicated the presence of undescribed species that are closely related to described bacteria, whereas others indicated the presence of new species or genera with little relatedness to known bacteria. How can this high diversity of the gut microbiota be explained? It can be assumed that the number of fermentable substrates available to the bacteria in the gastrointestinal tract is a major reason for the complexity of the microbial community in the intestine. Not only the substrates originating from the diet or the host but also the large number of intermediates formed during bacterial breakdown of indigestible dietary components contribute to the large variety of substrates. The main substrates available to the bacteria in the human colon are dietary carbohydrates that have escaped digestion in the small intestine (3). These include resistant starches, dietary fiber (cellulose, hemicellulose, pectin, inulin), and unabsorbed sugars and sugar alcohols. However, dietary protein and protein from pancreatic enzymes and gastrointestinal secretions also contribute to some extent to the supply of substrates to intestinal bacteria (4). Mucus produced by the host and sloughed epithelial cells are other potential substrates.
The fermentation of complex polymers such as polysaccharides and proteins in the colon requires the cooperative action of different microbial population groups. The breakdown starts with the depolymerization of complex carbohydrates and proteins and gives rise to mono- and oligomeric compounds that can be broken down further to the short-chain fatty acids (SCFA) acetate, propionate, and butyrate as well as to carbon dioxide and molecular hydrogen. Lactic acid, ethanol, succinic acid, and formate are important intermediates that are also degraded to SCFA, CO2, and H2. Proteins are broken down to peptides and amino acids, whose fermentation also results in the formation of SCFA, CO2, and H2. In addition, branched-chain fatty acids, ammonia, hydrogen sulfide, amines, phenols, indoles, and mercaptanes are formed (4).
Microbial activities and their relevance to health and disease
Formation of short-chain fatty acids. The formation of SCFA is of major relevance to the host. The daily production of SCFA has been estimated to be in the range of 400 mmol (5). The bacterial formation of SCFA enables the host to salvage some of the energy contained in dietary fiber that would be lost otherwise. Various tissues in the body are able to oxidize SCFA for energy generation. Butyrate is the preferred fuel of the colon epithelial cells that derive 70% of their energy from the oxidation of butyrate (6).
Butyrate has been proposed to lower the risk of colon cancer. This notion is based on a number of observations including the ability of butyrate to inhibit the genotoxic activity of nitrosamides and hydrogen peroxide in human colon cells (7) and the potential of butyrate to induce apoptosis in human colonic tumor cell lines in a p53-independent pathway (8). It has also been proposed that butyrate plays a major role in chronic inflammation of the intestinal mucosa. The inability of the colonocytes to oxidize butyrate was considered as a possible reason. In accordance with this notion, colon epithelial cells from ulcerative colitis (UC) patients were reported to have a reduced capacity to oxidize SCFA (9). However, more recent work has shown that the reduced butyrate oxidation rate observed in patients with active UC is reversed during remission, suggesting that UC mucosa is not intrinsically altered in butyrate oxidation and making the inability to oxidize butyrate unlikely to be a primary defect in UC (10). Nevertheless, SCFA irrigation for 2 to 3 wk has been shown to improve the macroscopic and histological signs of inflammation resulting from diversion colitis, which develops after complete diversion of the fecal stream (11). It is conceivable that butyrate acts at least partially via its effect on mediators of inflammation. Butyrate was shown to decrease the expression of the proinflammatory cytokines tumor necrosis factor-
(TNF-), TNF-ß, interleukin-6 (IL-6), and IL-1ß by inhibiting the activation of nuclear factor 
B (NF-B) in lamina propria mononuclear cells from patients with Crohn's disease (12). Similarly, butyrate inhibits NF-B activation in lamina propria macrophages of patients with UC and results in a significant decrease in the disease activity index in these patients (13).
Protein and amino acid fermentation in the colon. Whereas the bacterial conversion of fermentable carbohydrates occurs primarily in the proximal colon, the fermentation of proteins occurs mainly in the distal colon (4). Some of the products resulting from amino acid fermentation have some relevance to health. Oxidative or reductive deamination of amino acids leads to the formation of ammonia, whereas decarboxylation results in the production of amines. High ammonia concentrations have been shown to act as tumor promoters (14): Rats were treated with N-methyl-N'-nitro-N-nitrosoguanidine to induce tumors and subsequently assigned to either the control group or to the ammonium acetate treatment group. Sixty-nine percent of the animals in the treatment group had 28 adenocarcinomas, 8 of which were invasive, whereas only 40% of control animals had 12 adenocarcinomas, none of which was invasive.
The bacterial degradation of the amino acids cysteine and methionine results in the formation of H2S (present as HS– at neutral pH). A diet rich in meat correlates with high fecal concentrations of sulfide (15). H2S is toxic and was shown to inhibit butyrate oxidation in colonocytes (16). It was subsequently proposed that H2S could play a role in UC (17). Sulfate-reducing bacteria (SRB) were identified as another major source of H2S. SRB couple the oxidation of lactate, ethanol, succinate, and H2 to the reduction of sulfate to sulfide. Foods may contain high levels of oxidized forms of sulfur such as sulfate, sulfite, bisulfite, and sulfur dioxide. These food additives as well as endogenous sulfated mucins are potential sources of bacterial sulfide formation (18). A variety of morphologically and nutritionally different SRB were isolated from human feces and found to belong to 5 different genera with Desulfovibrio being the dominant genus (19).
The decarboxylation of amino acids in the colon results in the formation of amines. Under acidic conditions or catalyzed by intestinal bacteria, the latter may react with nitrite to form N-nitroso compounds. Many oral and intestinal bacteria are capable of reducing nitrate to nitrite. However, it is not clear whether bacterial nitrite is a key agent in nitrosation. In any case, the gut microbiota have the capacity to catalyze the formation of nitrosamines from secondary amines and nitrite (20). Nitrosamines are highly carcinogenic.
The anaerobic fermentation of the aromatic amino acids tyrosine and tryptophan by colonic bacteria gives rise to phenols and indoles, respectively, which are eventually excreted in the urine (4). Urinary indoles and phenols are increased in response to a protein-rich diet (21). Phenols such as p-cresol have been proposed to act as procarcinogens in colon cancer (22). N-Nitrosation of dimethylamine by nitrite is enhanced by phenol, and the reaction of phenol with nitrite produces p-nitrosophenol and p-diazoquinone, both of which are cancerogenic (23).
Transformation of bile acids and xenobiotics.
Bile acids are secreted as glycine, taurine, or sulfate conjugates. These undergo deconjugation followed by a dehydroxylation reaction. For example, the deconjugation of glycocholate leads to cholate, which in turn is transformed by bacterial 7-dehydroxylase to deoxycholate, 1 of the so-called secondary bile acids. There are good indications that secondary bile acids may act as tumor promoters (24).
Dietary components, pharmaceuticals, and endogenous metabolites with hydrophobic properties are transported to the liver, where they undergo oxidation by the cytochrome P450 system, resulting in the corresponding hydroxyl compounds. The latter are subsequently conjugated with either glucuronic acid, sulfate, or glutathione to increase their water solubility and facilitate their urinary or biliary excretion. Compounds excreted in bile reach the intestinal tract, where they undergo deconjugation by intestinal microorganisms. A large variety of gut microorganisms possess hydrolytic enzymes such as ß-glucuronidase and sulfatase (25). The deconjugated metabolites may be reabsorbed, entering the enterohepatic circulation.
Bacterial degradation of oxalate in the intestine. Oxalobacter formigenes is present in the human intestinal tract, where it lives at the expense of the transformation of oxalate to formate and carbon dioxide (26). It has been shown that the absence of O. formigenes is a risk factor for the formation of calcium oxalate stones (urolithiasis) (27) and that calcium oxalate stone formers have a low rate of colonization with O. formigenes (28). Moreover, the oral uptake of O. formigenes by human volunteers reduces the urinary oxalate excretion and results in oxalate-degrading activity in feces (29).
Activation and inactivation of bioactive food components. The human diet contains a large variety of plant-derived nonnutritive substances including lignans and flavonoids, which belong to the large group of polyphenols. Following their uptake with the diet, these compounds may be absorbed to some extent, but they may also undergo transformation by intestinal bacteria. The biological properties of the resulting transformation products may differ considerably from those of the original compound. The bacterial transformation of a bioactive compound may result in the formation of an inactive compound. Alternatively, the activity may be enhanced as a result of bacterial transformation, and an originally inactive compound may be activated through bacterial conversion.
Isoflavonoids, which are found for instance in soy, beer, or clover, have been reported to have estrogenic properties. Together with lignans (see below), they are called phytoestrogens, and, based on their purported biological effects, they have been proposed to be chemoprotective agents. The plasma concentrations of the flavonoids daidzein and genistein appear to be highly influenced by diet. Whereas the plasma concentration of daidzein and genistein was reported to be 383 nmol/L in Japanese men, it was only 12.5 nmol/L in Finnish men (30). This can be related to the high consumption of soy and soy products in Japan. Isoflavones have been associated with a number of health effects (31,32). These include the prevention of hormone-related cancers such as breast cancer, atherosclerosis, and osteoporosis in the alleviation of menopausal symptoms. Their inhibitory effect on tyrosine-specific protein kinases and on topoisomerases I and II, which influence cell proliferation, has been proposed as a possible mechanism of their action (33,34). It has been shown that the isoflavone daidzein undergoes transformation by intestinal bacteria to form products with either reduced or enhanced biological activity. In the human gastrointestinal tract, daidzein may undergo bacterial transformation to equol, which has a higher biological activity than daidzein (35,36). It is interesting to note that approximately 1 of 3 individuals produces equol (37). Alternatively, daidzein may also be degraded to O-demethylangolensin (DMA) (38), which in contrast to daidzein or equol is biologically inactive. The organism(s) catalyzing the formation of equol are not yet known. Eubacterium ramulus, which has become known for its ability to metabolize a number of flavonoids including quercetin, apigenin, and naringenin (39,40), was shown to convert daidzein to DMA, which, however, is not degraded any further by this organism (41). In contrast, the degradation of genistein by E. ramulus continues beyond the intermediate 6'-hydroxy-DMA. The latter undergoes cleavage to 4-hydroxyphenyl-2-propionic acid and phloroglucinol (41).
Plant lignans, e.g., secoisolariciresinol diglucoside, are converted by human intestinal bacteria to the enterolignans enterodiol and enterolactone. Therefore, bacteria influence the possible beneficial health effects of these active estrogen-like compounds. Lignans have been reported to have estrogenic and antioxidant activities (42,43). They may act through their ability to bind to proteins or inhibit relevant enzymes (44–46). In rats, lignans have been shown to reduce mammary tumor growth at various stages of carcinogenesis (47). However, evidence from human studies for a cancer preventive effect is insufficient (48,49). There are good indications that lignans have protective effects against diabetes (50) and coronary heart disease by their hypocholesterolemic and antiatherogenic effects (51).
Recently, we have used culture-based and molecular approaches to investigate the diversity and occurrence of lignan-transforming intestinal bacteria. In contrast to the bacterial production of equol, which is observed in 30% of human individuals, the conversion of secoisolariciresinol to enterodiol and enterolactone is widely distributed among human subjects. Eleven phylogenetically and functionally distantly related bacterial species that catalyze the O-deglycosylation, O-demethylation, dehydroxylation, or dehydrogenation step of secoisolariciresinol diglucoside have been isolated from human feces or obtained from bacterial culture collections (52). Most of these species are members of dominant intestinal microbiota, as determined by most probable number and fluorescent in situ hybridization enumerations (53,54). They include strains of the genera Bacteroides, Clostridium, Eggerthella, Eubacterium, and Ruminococcus. The in vitro transformation of secoisolariciresinol diglucoside to enterolactone has been demonstrated using a defined mixed culture of bacteria (Fig. 1). The challenge is now to bring to the test the relevance of these in vitro findings using animal models and to see how changes in bacterial population levels in the intestinal tract may influence the bioavailability and health effects of lignans.
|
|
FOOTNOTES |
|---|
2 Author disclosure: no relationships to disclose.
3 Abbreviations used: cfu, colony-forming unit; DMA, O-demethylangolensin; SCFA, short-chain fatty acids; SRB, sulfate-reducing bacteria; UC, ulcerative colitis.
|
LITERATURE CITED |
|---|
|
TOPABSTRACTLITERATURE CITED |
|---|
1. Blaut M, Collins MD, Welling GW, Dore J, van Loo J, de Vos W. Molecular biological methods for studying the gut microbiota: the EU human gut flora project. Br J Nutr. 2002;87: Suppl 2:S203–11.
2. Suau A, Bonnet R, Sutren M, Godon JJ, Gibson GR, Collins MD, Dore J. Direct analysis of genes encoding 16S rRNA from complex communities reveals many novel molecular species within the human gut. Appl Environ Microbiol. 1999;65:4799–807.
3. Cummings JH, Macfarlane GT. Colonic microflora: nutrition and health. Nutrition. 1997;13:476–8.[Medline]
4. Macfarlane S, Macfarlane GT. Proteolysis and amino acid fermentation. In: Gibson GR, Macfarlane GT, editors. Human colonic bacteria: role in nutrition, physiology and pathology. Boca Raton: CRC Press; 1995. p. 75–100.
5. Cummings J. Quantitative short chain fatty acid production in humans. In: Cummings J, Binder HJ, Soergel K, editors. Short-chain fatty acids. Boston: Kluwer Academic Publisher; 1994.
6. Roediger WE. Role of anaerobic bacteria in the metabolic welfare of the colonic mucosa in man. Gut. 1980;21:793–8.
7. Wollowski I, Rechkemmer G, Pool-Zobel BL. Protective role of probiotics and prebiotics in colon cancer. Am J Clin Nutr. 2001;73: 2 Suppl:451S–5S.
8. Hague A, Manning AM, Hanlon KA, Huschtscha LI, Hart D, Paraskeva C. Sodium butyrate induces apoptosis in human colonic tumour cell lines in a p53-independent pathway: implications for the possible role of dietary fibre in the prevention of large-bowel cancer. Int J Cancer. 1993;55:498–505.[Medline]
9. Roediger WE. The colonic epithelium in ulcerative colitis: an energy-deficiency disease? Lancet. 1980;2:712–5.[Medline]
10. Den Hond E, Hiele M, Evenepoel P, Peeters M, Ghoos Y, Rutgeerts P. In vivo butyrate metabolism and colonic permeability in extensive ulcerative colitis. Gastroenterology. 1998;115:584–90.[Medline]
11. Harig JM, Soergel KH, Komorowski RA, Wood CM. Treatment of diversion colitis with short-chain-fatty acid irrigation. N Engl J Med. 1989;320:23–8.[Abstract]
12. Segain JP, Raingeard de la Bletiere D, Bourreille A, Leray V, Gervois N, Rosales C, Ferrier L, Bonnet C, Blottiere HM, Galmiche JP. Butyrate inhibits inflammatory responses through NFkappaB inhibition: implications for Crohn's disease. Gut. 2000;47:397–403.
13. Luhrs H, Gerke T, Muller JG, Melcher R, Schauber J, Boxberge F, Scheppach W, Menzel T. Butyrate inhibits NF-kappaB activation in lamina propria macrophages of patients with ulcerative colitis. Scand J Gastroenterol. 2002;37:458–66.[Medline]
14. Clinton SK, Bostwick DG, Olson LM, Mangian HJ, Visek WJ. Effects of ammonium acetate and sodium cholate on N-methyl-N'-nitro-N-nitrosoguanidine-induced colon carcinogenesis of rats. Cancer Res. 1988;48:3035–9.
15. Magee EA, Richardson CJ, Hughes R, Cummings JH. Contribution of dietary protein to sulfide production in the large intestine: an in vitro and a controlled feeding study in humans. Am J Clin Nutr. 2000;72:1488–94.
16. Roediger WE, Duncan A, Kapaniris O, Millard S. Reducing sulfur compounds of the colon impair colonocyte nutrition: implications for ulcerative colitis. Gastroenterology. 1993;104:802–9.[Medline]
17. Pitcher MC, Cummings JH. Hydrogen sulphide: a bacterial toxin in ulcerative colitis? Gut. 1996;39:1–4.
18. Florin T, Neale G, Gibson GR, Christl SU, Cummings JH. Metabolism of dietary sulphate: Absorption and excretion in humans. Gut. 1991;32:766–73.
19. Gibson GR, Macfarlane GT, Cummings JH. Occurrence of sulphate-reducing bacteria in human faeces and the relationship of dissimilatory sulphate reduction to methanogenesis in the large gut. J Appl Bacteriol. 1988;65:103–11.[Medline]
20. Hecht SS. Approaches to cancer prevention based on an understanding of N-nitrosamine carcinogenesis. Proc Soc Exp Biol Med. 1997;216:181–91.[Abstract]
21. Geypens B, Claus D, Evenepoel P, Hiele M, Maes B, Peeters M, Rutgeerts P, Ghoos Y. Influence of dietary protein supplements on the formation of bacterial metabolites in the colon. Gut. 1997;41:70–6.
22. Bone E, Tamm A, Hill M. The production of urinary phenols by gut bacteria and their possible role in the causation of large bowel cancer. Am J Clin Nutr. 1976;29:1448–54.
23. Kikugawa K, Kato T. Formation of a mutagenic diazoquinone by interaction of phenol with nitrite. Food Chem Toxicol. 1988;26:209–14.[Medline]
24. Summerton J, Goeting N, Trotter GA, Taylor I. Effect of deoxycholic acid on the tumour incidence, distribution, and receptor status of colorectal cancer in the rat model. Digestion. 1985;31:77–81.[Medline]
25. McBain AJ, Macfarlane GT. Ecological and physiological studies on large intestinal bacteria in relation to production of hydrolytic and reductive enzymes involved in formation of genotoxic metabolites. J Med Microbiol. 1998;47:407–16.[Abstract]
26. Allison MJ, Dawson KA, Mayberry WR, Foss JG. Oxalobacter formigenes gen. nov., sp. nov.: Oxalate-degrading anaerobes that inhabit the gastrointestinal tract. Arch Microbiol. 1985;141:1–7.[Medline]
27. Sidhu H, Schmidt ME, Cornelius JG, Thamilselvan S, Khan SR, Hesse A, Peck AB. Direct correlation between hyperoxaluria/oxalate stone disease and the absence of the gastrointestinal tract-dwelling bacterium Oxalobacter formigenes: Possible prevention by gut recolonization or enzyme replacement therapy. J Am Soc Nephrol. 1999;10: Suppl 14:S334–40.
28. Troxel SA, Sidhu H, Kaul P, Low RK. Intestinal Oxalobacter formigenes colonization in calcium oxalate stone formers and its relation to urinary oxalate. J Endourol. 2003;17:173–6.[Medline]
29. Duncan SH, Richardson AJ, Kaul P, Holmes RP, Allison MJ, Stewart CS. Oxalobacter formigenes and its potential role in human health. Appl Environ Microbiol. 2002;68:3841–7.
30. Uehar M, Arai Y, Watanabe S, Adlercreutz H. Comparison of plasma and urinary phytoestrogens in Japanese and Finnish women by time-resolved fluoroimmunoassay. Biofactors. 2000;12:217–25.[Medline]
31. Birt DF, Hendrich S, Wang W. Dietary agents in cancer prevention: flavonoids and isoflavonoids. Pharmacol Ther. 2001;90:157–77.[Medline]
32. Adlercreutz H, Mazur W. Phyto-oestrogens and Western diseases. Ann Med. 1997;29:95–120.[Medline]
33. Akiyama T, Ishida J, Nakagawa S, Ogawara H, Watanabe S, Itoh N, Shibuya M, Fukami Y. Genistein, a specific inhibitor of tyrosine-specific protein kinases. J Biol Chem. 1987;262:5592–5.
34. Okura A, Arakawa H, Oka H, Yoshinari T, Monden Y. Effect of genistein on topoisomerase activity and on the growth of [Val 12]Ha-ras-transformed NIH 3T3 cells. Biochem Biophys Res Commun. 1988;157:183–9.[Medline]
35. Chang YC, Nair MG. Metabolism of daidzein and genistein by intestinal bacteria. J Nat Prod. 1995;58:1892–6.[Medline]
36. Chang YC, Nair MG, Nitiss JL. Metabolites of daidzein and genistein and their biological activities. J Nat Prod. 1995;58:1901–5.[Medline]
37. Rowland IR, Wiseman H, Sanders TA, Adlercreutz H, Bowey EA. Interindividual variation in metabolism of soy isoflavones and lignans: influence of habitual diet on equol production by the gut microflora. Nutr Cancer. 2000;36:27–32.[Medline]
38. Heinonen S, Wahala K, Adlercreutz H. Identification of isoflavone metabolites dihydrodaidzein, dihydrogenistein, 6'-OH-O-DMA, and cis-4-OH-equol in human urine by gas chromatography-mass spectroscopy using authentic reference compounds. Anal Biochem. 1999;274:211–9.[Medline]
39. Braune A, Gutschow M, Engst W, Blaut M. Degradation of quercetin and luteolin by Eubacterium ramulus. Appl Environ Microbiol. 2001;67:5558–67.
40. Blaut M, Schoefer L, Braune A. Transformation of flavonoids by intestinal microorganisms. Int J Vitam Nutr Res. 2003;73:79–87.[Medline]
41. Schoefer L, Mohan R, Braune A, Birringer M, Blaut M. Anaerobic C-ring cleavage of genistein and daidzein by Eubacterium ramulus. FEMS Microbiol Lett. 2002;208:197–202.[Medline]
42. Mousavi Y, Adlercreutz H. Enterolactone and estradiol inhibit each other's proliferative effect on MCF-7 breast cancer cells in culture. J Steroid Biochem Mol Biol. 1992;41:615–9.[Medline]
43. Kitts DD, Yuan YV, Wijewickreme AN, Thompson LU. Antioxidant activity of the flaxseed lignan secoisolariciresinol diglycoside and its mammalian lignan metabolites enterodiol and enterolactone. Mol Cell Biochem. 1999;202:91–100.[Medline]
44. Mueller SO, Simon S, Chae K, Metzler M, Korach KS. Phytoestrogens and their human metabolites show distinct agonistic and antagonistic properties on estrogen receptor (ER){alpha} and ER{beta} in human cells. Toxicol Sci. 2004;80:14–25.
45. Adlercreutz H, Bannwart C, Wahala K, Makela T, Brunow G, Hase T, Arosemena PJ, Kellis JT Jr, Vickery LE. Inhibition of human aromatase by mammalian lignans and isoflavonoid phytoestrogens. J Steroid Biochem Mol Biol. 1993;44:147–53.[Medline]
46. Schottner M, Gansser D, Spiteller G. Lignans from the roots of Urtica dioica and their metabolites bind to human sex hormone binding globulin (SHBG). Planta Med. 1997;63:529–32.[Medline]
47. Thompson LU. Experimental studies on lignans and cancer. Baillieres Clin Endocrinol Metab. 1998;12:691–705.[Medline]
48. Demark-Wahnefried W, Robertson CN, Walther PJ, Polascik TJ, Paulson DF, Vollmer RT. Pilot study to explore effects of low-fat, flaxseed-supplemented diet on proliferation of benign prostatic epithelium and prostate-specific antigen. Urology. 2004;63:900–4.[Medline]
49. Thompson LU, Chen JM, Li T, Strasser-Weippl K, Goss PE. Dietary flaxseed alters tumor biological markers in postmenopausal breast cancer. Clin Cancer Res. 2005;11:3828–35.
50. Prasad K. Secoisolariciresinol diglucoside from flaxseed delays the development of type 2 diabetes in Zucker rat. J Lab Clin Med. 2001;138:32–9.[Medline]
51. Prasad K. Flaxseed: a source of hypocholesterolemic and antiatherogenic agents. Drug News Perspect. 2000;13:99–104.[Medline]
52. Clavel T, Henderson G, Engst W, Doré J, Blaut M. Phylogeny of human intestinal bacteria that activate the dietary lignan secoisolariciresinol diglucoside. FEMS Microbiol Ecol. 2006;55:471–78.[Medline]
53. Clavel T, Borrmann D, Braune A, Doré J, Blaut M. Occurrence and activity of human intestinal bacteria involved in the conversion of dietary lignans. Anaerobe. 2006;12:140–7.[Medline]
54. Clavel T, Henderson G, Alpert C-A, Philippe C, Rigottier-Gois L, Dore J, Blaut M. Intestinal bacterial communities that produce active estrogen-like compounds enterodiol and enterolactone in humans. Appl Environ Microbiol. 2005;71:6077–85.
This article has been cited by other articles:
|
|
 |
|
  M. Membrez, F. Blancher, M. Jaquet, R. Bibiloni, P. D. Cani, R. G. Burcelin, I. Corthesy, K. Mace, and C. J. Chou Gut microbiota modulation with norfloxacin and ampicillin enhances glucose tolerance in mice FASEB J, July 1, 2008; 22(7): 2416 - 2426. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Are, L. Aronsson, S. Wang, G. Greicius, Y. K. Lee, J.-A. Gustafsson, S. Pettersson, and V. Arulampalam Enterococcus faecalis from newborn babies regulate endogenous PPAR{gamma} activity and IL-10 levels in colonic epithelial cells PNAS, February 12, 2008; 105(6): 1943 - 1948. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
) secoisolariciresinol glucoside, (
) demethyl-secoisolariciresinol, (x) didemethyl-secoisolaricresinol, (
) 2,3-bis(3,4-dihydroxybenzyl)butyro-lactone. For these metabolites, the Y-values are the signal intensities measured at 285 nm by the UV diode array detector of the HPLC system. Resting cells were prepared as described previously (
109 cells/mL.