Increased serum deoxycholic acid levels in men with colorectal adenomas

Bayerdörffer, Ekkehard; Mannes, G. A.; Richter, Werner; Ochsenkühn, Thomas; Wiebecke, B; Köpcke, Wolfgang; Paumgartner, Gustav

doi:10.1016/0016-5085(93)90846-5

Cited by 217 publications

(125 citation statements)

References 41 publications

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“…81 Rats fed 20% corn oil or lard secreted significantly more fecal bile acids, and were more susceptible to colon cancer than rats fed normal levels of dietary fat (5%) in a 1,2-dimethylhydrazine-induced model. 82 In the 1990s it was shown that: i) DCA was significantly elevated in serum of patients with colorectal adenomas; [83][84][85] ii) serum DCA correlates with DCA in fecal water; 83 and iii) colonic mucosal proliferation is correlated with DCA in serum. 86 The activation of cellular signaling cascades and membrane perturbing effects generated by secondary bile acids, but not primary bile acids, provide mechanisms by which DCA and LCA promote CRC.…”

Section: Deoxycholic Acid and Colon Cancermentioning

confidence: 99%

Taurocholic acid metabolism by gut microbes and colon cancer

Ridlon¹,

Wolf²,

Gaskins³

2016

Gut Microbes

250

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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Section: Deoxycholic Acid and Colon Cancermentioning

confidence: 99%

Taurocholic acid metabolism by gut microbes and colon cancer

Ridlon¹,

Wolf²,

Gaskins³

2016

Gut Microbes

250

229

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“…The absorption of DCA from the large bowel is also age-dependent [15,16], higher in adenoma patients than in age-matched controls, and coincides with a more anaerobic environment [17,18]. One study showed a higher biliary CDCA fraction in adenoma and carcinoma patients [19], Recently it was demonstrated that adenoma pati ents have a higher serum DCA concentration than healthy controls [20,21].…”

Section: Epidemiologymentioning

confidence: 99%

Role of bile acids in colorectal carcinogenesis

Nagengast

Grubben

Munster

1995

European Journal of Cancer

315

180

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Dietary factors are considered important environmental risk determinants for colorectal cancer development. Epidemiological studies have shown that a high fat (or meat) intake is associated positively and a high starch, fibre (non-starch polysaccharide), vegetable and fruit intake negatively with colorectal cancer incidence. One mechanism by which these effects are possibly exerted is through the metabolism of secondary bile acids. Secondary bile acids are formed after enzymatic deconjugation and dehydroxylation of primary bile acids in the large bowel by anaerobic bacteria. It has been shown that these compounds can have tumour-promoting capacities in animal experiments. In epidemiological studies, colonic cancer risk is related to the faecal bile acid concentration. In serum and bile of patients with colonic adenomas, more deoxycholic acid was detected than in healthy controls. Secondary bile acids are toxic to several cell systems at physiological concentrations. The exact mechanism by which these amphiphilic molecules exert their action is not well understood. It might act through membrane damage, intracellular mitochondrial action or genotoxic effects. So far the evidence that bile acids are involved in colonic carcinogenesis is largely circumstantial. It is, however, well accepted that environmental factors, such as dietary habits influence genetic susceptibility. Bile acids could play a promoting role in this process.

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“…High fat diet and cholesterol are important risk factors for the emergence of colorectal cancers, presumably because of their associated impact on the synthesis and secretion of BA (Hill et al, 1971;Reddy, 1981;Willett et al, 1990;Nagengast et al, 1995). Several epidemiologic studies have implicated the alterations of the production and composition of BA in the intestinal lumen and blood with the increased incidence of colorectal adenomas and adenocarcinomas (McMichael and Potter, 1985;Bayerdo¨rffer et al, 1993;Owen, 1997;Kamano et al, 1999). Compelling evidence for a causal link between BA and colon cancer was supported by experimental carcinogenesis in rats.…”

Section: Introductionmentioning

confidence: 99%