Disease relevance of Coprosterol

• The fecal excretion of cholesterol, coprostanol, and cholestane-3beta, 5alpha, 6beta-triol was higher in patients with ulcerative colitis than in other groups [1].
• Coprostanol was decreased in shigellosis (12.2 +/- 8.2 versus 65.8 +/- 4.7% in controls, P less than 0.001) [2].
• The amount of total fecal neutral sterols and the percentage of fecal coprostanol were also markedly higher in the colon cancer group than in the controls [3].
• A plasmalogen, plasmenylethanolamine, is required for in vitro growth of strains of Eubacterium which convert cholesterol to coprostanol [4].
• A strong logarithmic correlation between the concentrations of E. coli and coprostanol was demonstrated in all surveys [5].

High impact information on Coprosterol

• The neutral sterols cholesterol, coprostanol, and coprostanone showed relatively similar, moderate inhibitory effects [6].
• Scarcely any coprostanol was found in the feces [7].
• Additionally, the following microflora-associated characteristics were studied in all the faecal samples: presence of short chain fatty acids, absence of beta-aspartylglycine, production of coprostanol, formation of urobilinogen, inactivation of tryptic activity and breakdown of mucin [8].
• Effect of environmental factors on the relationship between concentrations of coprostanol and fecal indicator bacteria in tropical (Mekong Delta) and temperate (Tokyo) freshwaters [5].
• METHODS: Microflora associated characteristics (MACs) were assessed by determining the concentrations of eight different short chain fatty acids and the conversion of cholesterol to coprostanol by gas chromatography [9].

Chemical compound and disease context of Coprosterol

• However, the coprostanol ratio and the urobilinogen level were lower and the FTA was higher in patients with colitis than in the controls (p < 0.05) [10].
• 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 [11].

Biological context of Coprosterol

• The initiation of the establishment of conversion was delayed by breast-feeding, and only one child had coprostanol in feces while still being breast-fed [12].
• The relationship between the concentrations of fecal sterols and bacterial indicators was examined in an attempt to develop public health criteria for coprostanol levels applicable to the tropical region [13].
• The esterification of sterols was facilitated by the presence of a 3beta-hydroxyl group and the trans configuration of the A/B rings, as was evident from the lack of acceptor activity of all 3 alpha-hydroxy sterols tested and coprostanol [14].
• Bioindicators of health (lipid content), condition and gonad indices (CI and GI), and sex ratio, as well as vitellins, were compared with the bioaccumulation of polycyclic aromatic compounds (PACs) including polycyclic aromatic hydrocarbons (PAHs), polychlorinated biphenyls (PCBs), coprostanol, and metals [15].
• A reduction in bacterial transformation of cholesterol to coprostanol and coprostanone was observed which lasted 1-2 weeks after 5 days' intake of oxytetracycline (1000 mg/day) [16].

Anatomical context of Coprosterol

• Contents from different parts of the intestine were investigated with regard to the following microflora-associated characteristics: degradation of mucin, beta-aspartylglycine and tryptic activity, conversion of cholesterol to coprostanol and bilirubin to urobilinogen, deconjugation of bilirubin glucuronides, and reduction of the cecum size [17].
• The addition of sodium taurocholate (0.2, 0.75, and 4%) strongly reduced coprostanol formation, while a chronic bile duct ligation led to an enhancement [18].
• In an earlier study, freshwater mussels exposed to contaminated river water for 62 days accumulated large quantities of coprostanol (Cop) in their soft tissues (16 micrograms/g dry wt.). Moreover, these mussels were found to have elevated levels of vitellin in their hemolymphs, suggesting estrogenic effects [19].
• Plasma cholesterol concentration of experimental rabbits (183.3 +/- 11.0 mg dl-1, mean +/- S.E.) was significantly lower (P < 0.001) than that of controls (248.8 +/- 12.3 mg dl-1, mean +/- S.E.). The coprostanol-to-cholesterol ratios in contents of digestive tracts of experimental rabbits were greater than those of controls [20].
• The purpose of this study was to examine the cytotoxic and oxidative effects of these products and other wastewater-related products (i.e., coprostanol, cotinine, estradiol-17beta, nonylphenol, and cholesterol) in primary cultures of rainbow trout hepatocytes [21].

Associations of Coprosterol with other chemical compounds

• The submarine outfalls in Hong Kong represent important sources of the sewage pollution to the Pearl River estuarine sediments evidenced by a combination of coprostanol concentration, diagnostic indices, sterol profiles and UCM [22].
• Conversion to coprostanol, conversion to urobilinogens and degradation of mucin were affected by treatment of zinc bacitracin and conversion to coprostanol was most sensitive [23].
• Microbial conversion of cholesterol to coprostanol, bilirubin to urobilinogen and 7-alpha-dehydroxylation of cholic acid have been investigated to evaluate hepatic/intestinal co-functions, and degradation of intestinal mucin in order to evaluate the integrity in the intestinal mucosa [24].
• The subjects whose feces contained smaller amount of coprostanol excreted larger amounts of beta-sitosterol and crude fiber, suggesting that the various activities of intestinal flora were lower than the other subjects [25].
• Stigmasterol, coprostanol and epicholesterol cause only minor alterations in both translocation and interfacial processes [26].

Gene context of Coprosterol

• Our results show that conversion of cholesterol to coprostanol was present in all horses, irrespective of diet [27].
• The results indicate that patients with RA have an abnormal formation of coprostanol, which is ascribed to alterations in the function of the Eubacteria species [28].

Analytical, diagnostic and therapeutic context of Coprosterol

• The same was true of six of the 10 patients with continent ileostomies; in the other four patients at least 10% of acidic or neutral steroids were excreted as secondary bile acids or as a coprostanol [29].
• Results from using the HPLC method to analyze a sediment reference material for coprostanol were statistically comparable to a previously used gravity-flow column method [30].
• The effect of enteral nutrition (EN) on the following seven intestinal microflora-associated characteristics (MACs) was studied: formation of urobilinogen, coprostanol and deoxycholic acid, degradation of mucin and beta-aspartylglycine, faecal tryptic activity, and production of short-chain fatty acids (SCFAs) [31].
• Because coprostanol is absorbed poorly, it was hypothesized that oral administration of Eu. coprostanoligenes might decrease cholesterol concentration in blood because the micro-organisms will decrease the absorption of endogenous and dietary cholesterol by conversion to coprostanol [20].
• After bacterial feeding, the coprostanol to cholesterol ratio in feces of the active group was significantly greater than ratios of the inactive and control groups, indicating that E. coprostanoligenes was colonized in the intestine of hens and was converting intestinal cholesterol to coprostanol [32].

References