Metabolic epidemiology of colon cancer:Fecal bile acids and neutral sterols in colon cancer patients and patients with adenomatous polyps

Reddy, Bandaru S.; Wynder, Ernst L.

doi:10.1002/1097-0142(197706)39:6<2533::aid-cncr2820390634>3.0.co;2-x

Cited by 372 publications

(131 citation statements)

References 19 publications

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“…Eight patients with non-malignant colonic disease have also been studied and were found to have a low (25%) incidence of NDC isolated from their faeces. DISCUSSION Hill's finding of significantly increased total FBA concentrations in patients presenting with colorectal cancer has been confirmed by Reddy & Wynder (1977). These authors reported a significant rise in total FBA when they studied American Caucasians with colonic cancer and adenomatous polyps.…”

Section: Resultsmentioning

confidence: 69%

“…The mean age and sex distribution of the colorectal cancer group (Table I) colorectal-cancer patients in similar studies in England (Hill et al, 1975) and the U.S.A. (Reddy & Wynder, 1977). The incidence of chronic irregular bowel habit (< 1 stool per 3 days or regular laxative use) and a family history of any type of cancer in the patients with colorectal cancer is shown in Table II.…”

Section: Resultsmentioning

confidence: 88%

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Faecal bile acids and clostridia in the aetiology of colorectal cancer

Murray¹,

Backwood²,

Trotter³

et al. 1980

Br J Cancer

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Summary.-This study was undertaken in an attempt to confirm the increased bileacid concentration in association with nuclear dehydrogenating Clostridia (NDC) in the faeces of colorectal cancer patients. We have studied 37 patients with colorectal cancer and 36 control patients with no known gastrointestinal disease. Stool specimens were obtained for biochemical analysis (total faecal bile acid (FBA), lithocholic deoxycholic and cholic acids) and NDC isolation. The mean total FBA concentration (tmol/g) in the control group was 20-5 + 22 (s.e.) significantly higher (P <0.001) than the colorectal -cancer group (11-8 + 0.7). There was no statistically significant difference in the percentage distribution of the individual FBAs measured. NDC were isolated from the faeces of 640O/ of colorectal-cancer patients and 15% of control patients, this difference being statistically significant (P<0.001). These results suggest that bacteria capable of metabolizing steroids may be implicated in the aetiology of colorectal cancer. However, the relationship between FBA and colorectal cancer requires further evaluation.

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Section: Resultsmentioning

confidence: 69%

Section: Resultsmentioning

confidence: 88%

Faecal bile acids and clostridia in the aetiology of colorectal cancer

Murray¹,

Backwood²,

Trotter³

et al. 1980

Br J Cancer

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“…and adenomas have higher total fecal bile acid levels, 70 resulting from animal protein and fat. 71 In developing countries, CRC rates were shown to be significantly higher in cities relative to rural areas, consistent with different dietary patterns.…”

Section: Deoxycholic Acid and Colon Cancermentioning

confidence: 99%

Taurocholic acid metabolism by gut microbes and colon cancer

Ridlon¹,

Wolf²,

Gaskins³

2016

Gut Microbes

264

229

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Colorectal cancer (CRC) is one of the most frequent causes of cancer death worldwide and is associated with adoption of a diet high in animal protein and saturated fat. Saturated fat induces increased bile secretion into the intestine. Increased bile secretion selects for populations of gut microbes capable of altering the bile acid pool, generating tumor-promoting secondary bile acids such as deoxycholic acid and lithocholic acid. Epidemiological evidence suggests CRC is associated with increased levels of DCA in serum, bile, and stool. Mechanisms by which secondary bile acids promote CRC are explored. Furthermore, in humans bile acid conjugation can vary by diet. Vegetarian diets favor glycine conjugation while diets high in animal protein favor taurine conjugation. Metabolism of taurine conjugated bile acids by gut microbes generates hydrogen sulfide, a genotoxic compound. Thus, taurocholic acid has the potential to stimulate intestinal bacteria capable of converting taurine and cholic acid to hydrogen sulfide and deoxycholic acid, a genotoxin and tumor-promoter, respectively.

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“…Butyrate has been shown to increase apoptosis in both colon adenoma and cancer cell lines in a p53-independent way (Hague et al, 1993), an effect that is likely to contribute significantly to its protective effects. In contrast, a diet high in saturated fats is associated with an increased level of faecal secondary bile acids (Radley et al, 1993) and an increased risk of colorectal cancer (Reddy and Wynder, 1977). Secondary bile acids, deoxycholic acid (DCA), ursodeoxycholic acid (UDCA) and lithocholic acid, are produced by the actions of intestinal bacteria on primary bile acids.…”

mentioning

confidence: 99%

Opposing effects of butyrate and bile acids on apoptosis of human colon adenoma cells: differential activation of PKC and MAP kinases

et al. 2003

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Butyrate, produced in the colon by fermentation of dietary fibre, induces apoptosis in colon adenoma and cancer cell lines, which may contribute to protection against colorectal cancer. However, butyrate is present in the colon along with other dietary factors, including unconjugated bile acids, which are tumour promoters. We have shown previously that the proapoptotic effects of butyrate on AA/C1 human adenoma cells were reduced in the presence of bile acids. To determine the cellular basis of this interaction, we examined the effects of butyrate and the secondary bile acid ursodeoxycholic acid (UDCA) on signalling pathways known to regulate apoptosis using AA/C1 cells. Butyrate activated PKC-d and p38 MAP (mitogen-activated protein) kinase, whereas UDCA activated PKC-a and p42/44 MAP kinase. Butyrate treatment also resulted in the caspase-3-mediated proteolysis of PKC-d. Butyrate-induced apoptosis was reduced by inhibitors of PKC-d (Rottlerin), p38 MAP kinase (SB202190) and caspase 3 (DEVD-fmk), whereas the proliferative/survival effects of UDCA were blocked by inhibitors of PKC-a (Gö 6976) and MEK 1 (PD98059). The effects of butyrate and bile acids are therefore mediated by the differential activation of signalling pathways that are known to regulate apoptosis.

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Metabolic epidemiology of colon cancer:Fecal bile acids and neutral sterols in colon cancer patients and patients with adenomatous polyps

Cited by 372 publications

References 19 publications

Faecal bile acids and clostridia in the aetiology of colorectal cancer

Faecal bile acids and clostridia in the aetiology of colorectal cancer

Taurocholic acid metabolism by gut microbes and colon cancer

Opposing effects of butyrate and bile acids on apoptosis of human colon adenoma cells: differential activation of PKC and MAP kinases

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