A highly simplified method for plasma and fecal bile acid analysis in humans

Bile acid profiling in human biological samples: Comparison of extraction procedures and application to normal and cholestatic patients

“…The few previous studies from literature used GC-MS based on the assumption that fecal bile acids are mainly non-conjugated due to their active deconjugation by the microflora within the intestinal lumen [14][15][16]18,27,28], in accordance with these previous results, we found 97% of free bile acids in healthy patients. The two major bile acids found in stool were DCA (55% of total bile acids) and LCA (29%) in accordance with previous results [27].…”

“…Stool samples were thoroughly homogenized after reception and then stored at −80 • C. Before use, the samples were lyophilized, and 100 mg of dried stool were then treated according to 4 extraction protocols (S1-S4) [15][16][17][18], summarized in supplementary data 1B. Five microliter of the stock solution of the three internal standards were added to samples before extraction.…”

“…The four protocols tested used SPE extraction (for protocol comparison, see supplementary data 1B). NaOH extraction (S1 protocol) adapted from Perwaiz et al [15], and Batta et al [16] detected 15 molecular species and was used as the 100% reference method in Fig. 3D.…”

Vitamin D Receptor-dependent Regulation of Colon Multidrug Resistance-associated Protein 3 Gene Expression by Bile Acids

“…LCA is derived from the deconjugation and/or dehydroxylation of the primary bile acid CDCA at the C-7 position by intestinal bacteria (5,12). Unlike most primary bile acids that are efficiently reabsorbed in the ileum, LCA passes readily into the colon and is generally present at a level of 2-3.5 g/mg of fecal dry weight in healthy individuals (55). The data from the present study provide important new information regarding the mechanisms by which colon cells are protected against the high concentrations of this toxic bile acid.…”

Bile acids stimulate invasion and haptotaxis in human colorectal cancer cells through activation of multiple oncogenic signaling pathways

“…It is also tempting to speculate that UDCA might be useful in the treatment of colorectal cancer. Indeed, upon chronic administration, UDCA becomes the principal BA in bile, serum and stool (Kurtz, 1992;Batta et al, 1998), presumably through a negative feedback on BA synthesis. Consistent with this observation, feeding with UDCA in a rat model of colon carcinogenesis resulted in a decreased proportion of DCA in the stool, and absence of invasive tumors (Earnest et al, 1994).…”