Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A method is described for the analysis of fecal neutral steriods with a dual-column gas-liquid chromatography (GLC) system. After saponification of the fecal slurry, the neutral steroids were extracted with hexane. The GLC separation of the compounds and quantitation were achieved by simultaneous injection of the derivatized and derivatized aliquots of the extract onto dual colmuns under identical conditions. The neutral steroids of interest were than identified by matching the retention times with those of known standards, and identification was confirmed by use of an interfaced GLC high-resolution mass spectrometry system. The detection limit was 0.003 mg of steroid/g of fecal slurry. The pricision of the method is illustrated by a relative standard diviation of 2-10% and a recovery of neutral steroids from 73-96%. The method was applied to the determination of fecal neutral steroids in a "High protein diet in colon cancer study". A considerably larger level of coprostanone than of coprostanol was observed. Data on neutral steroids in fecal samples from subjects on different diets are the subject of a separate publication.
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PMID:Gas-liquid chromatography of fecal neutral steriods. 32 2

Because of potential significance of bile acids and cholesterol metabolites in the pathogenesis of colon cancer, fecal neutral sterols, and bile acids were determined in patients with colon cancer, adenomatous polyps or other digestive diseases and American or Japanese controls. The fecal excretion of cholesterol, coprostanol, coprostanone, total bile acids, deoxycholic acid, lithocholic acid was higher in patients with colon cancer and patients with adenomatous polyps compared to normal American and Japanese controls as well as patients with other digestive diseases. Patients with other digestive diseases excreted comparable levels of fecal bile acids and cholesterol metabolites compared to normal American controls; Japanese controls excreted reduced levels compared to normal American controls. These findings suggest that possible interactions between bile acids and cholesterol metabolites and colonic epithelial cells may be relevant in colon carcinogenesis.
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PMID:Metabolic epidemiology of colon cancer. Fecal bile acids and neutral sterols in colon cancer patients and patients with adenomatous polyps. 87 53

Epidemiological and experimental studies indicate a strong association between an elevated colon cancer risk and increased fecal excretion of secondary bile acids, neutral sterols, and prolonged gastrointestinal transit time. Starch malabsorption, on the other hand, has been reported to be a possible protective factor in colon carcinogenesis. To study the impact of starch malabsorption on these parameters, 12 healthy volunteers consumed a diet rich in starch for two 4-week periods. During a double-blind crossover trial they received the alpha-glucosidase inhibitor acarbose (BAY g 5421) in one of the study periods and placebo in the other. During acarbose treatment stool wet weight increased by 68%, stool dry weight by 57%, and gastrointestinal mean transit time by 30%. Fecal concentrations (mg/g dry weight) of the neutral sterols coprostanol, coprostanone, campesterol, 4-cholesten-3-one, and beta-sitosterol decreased by 36.8, 48.7, 42.1, 34.6, and 39.4%, respectively, under acarbose. Concentrations of the major secondary bile acids, deoxycholic and lithocholic acid, decreased by 59.9 and 52.2%, respectively. In spite of an increased stool weight, also daily excretion (mg/day) of these two bile acids was lower under acarbose (47.9 and 36.6%, respectively) compared to placebo, whereas excretion of the main primary bile acid, cholic acid, rose from 22.58 mg/day to 379.80 mg/day during the acarbose period. The changes in fecal bile acid and neutral sterol excretion found during acarbose treatment may explain a protective effect of starch malabsorption on colon cancer development.
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PMID:Effect of starch malabsorption on fecal bile acids and neutral sterols in humans: possible implications for colonic carcinogenesis. 186 44

Two components of human feces are known to induce nuclear anomalies in mice when applied intrarectally, but to be nonmutagenic in Salmonella. We have tested these two compounds for their ability to induce sister chromatid exchanges in the colonic epithelium of mice, the same tissue in which they induce nuclear anomalies when administered by the same route. One, 4-cholesten-3-one, induced sister chromatid exchanges whereas the other, 5-alpha-cholestan-3-one did not, even at the maximum feasible dose. The results suggest that 4-cholesten-3-one is more likely to be a significant factor in human colon cancer than the 5-alpha analog.
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PMID:Genotoxicity of two fecal steroids in murine colonic epithelium assessed by the sister chromatid exchange technique. 332 36

In previous studies subjects with familial polyposis, the autosomal dominant disease leading to colon cancer, excreted higher levels of fecal cholesterol than normal subjects, with decreased conversion to degradation products. Findings suggested fecal cholesterol degradation as a marker of hereditary predisposition to colon cancer. Current measurements now have shown that affected individuals and asymptomatic progeny in a second population group with inherited predisposition to colon cancer are low converters of fecal cholesterol. The latter group consisted of highly colon cancer prone families without polyposis, in which patterns of inheritance similar to the autosomal dominant pattern of familial polyposis were observed. 24-h stool collections were obtained from 72 subjects who consumed mixed western diets. Mean percent degradation of fecal cholesterol to coprostanol, coprostanone, cholestanol, and cholestanone revealed significant decreases in fecal cholesterol conversion in affected and asymptomatic subjects in colon cancer prone families without polyposis (P < 0.001) compared to controls. This is in addition to those with familial polyposis (P < 0.001), and extends this marker of colon cancer susceptibility to a second population group with hereditary predisposition to colonic neoplasia.
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PMID:Nondegradation of fecal cholesterol in subjects at high risk for cancer of the large intestine. 745 55

Diet-induced increases in fecal excretion of secondary bile acids (deoxy- and lithocholic acid) and certain neutral sterols (4-cholesten-3-one and 5a-cholestan-3-one) play a role in colon cancer development, whereas dietary fish oil (FO) has been implicated as a protective agent. In the present study the effects of FO and corn oil (CO) on these fecal parameters were investigated in 12 healthy volunteers consuming a low fat (30% of energy) controlled basal diet. After 4 weeks of FO supplementation (4.4 g omega-3 fatty acids/day), daily excretion of lithocholic acid showed a trend to lower values compared to CO consumption (p = 0.2), whereas other bile acids were not different during both study periods. Daily excretion of the putative colon carcinogen 4-cholesten-3-one was significantly lower in the FO compared to the CO period. This may be another biochemical mechanism by which FO exerts its protective effect on colon cancer development.
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PMID:Effect of dietary fish oil on fecal bile acid and neutral sterol excretion in healthy volunteers. 955 49