Postprandial concentrations of free and conjugated bile acids down the length of the normal human small intestine

Abstract

SUMMARY Small intestinal samples were obtained by intubation from multiple sites along the small intestine in 11 subjects with no known gastrointestinal disease eating a normal diet and at laparotomy in a further three subjects. Free (unconjugated) bile acids were consistently demonstrated in ileal samples, and occasionally in lower jejunal samples, by thin-layer chromatography, supplemented in some cases by gas/liquid chromatography and by infrared spectroscopy. The free bile acid concentration, measured enzymically following thin-layer chromatography, reached a maximum (1 mM) in the lower ileum, where it represented half the total bile acid concentration. Following ampicillin, the concentration of free bile acids decreased markedly, suggesting that they resulted from bacterial deconijugation; at the same time the total bile acid concentration increased, suggesting impaired absorption due to the reduced concentration of the more rapidly absorbed free bile acids. Our results indicate that the presence of free bile acids in lower jejunal and ileal samples is a normal finding, and cannot be taken as evidence of abnormal bacterial overgrowth. They also suggest that bacterial deconjugation at these sites may be a factor contributing to the remarkable efficiency of bile salt reabsorption.

Drug-Induced Perturbations of the Bile Acid Pool, Cholestasis, and Hepatotoxicity: Mechanistic Considerations beyond the Direct Inhibition of the Bile Salt Export Pump

“…Once formed, they can undergo extensive enzyme-catalyzed taurine and glycine conjugation to form (Table 1). Under normal conditions, such transport renders a very concentrated BA pool in the gallbladder (;100 mM total BAs) compared with liver tissue (;20 mM), small intestine lumen (2-10 mM), serum (;2 mM), and urine (;1 mM) (Northfield and McColl, 1973;Takikawa et al, 1985;GarciaCanaveras et al, 2012;Humbert et al, 2012). Via the bile ducts, BAs travel to the gallbladder and are released into the upper small intestine (duodenum).…”

“…1) (Trauner and Boyer, 2003;Ridlon et al, 2006;Ballatori et al, 2009;Gonzalez, 2012). Any taurine-or glycineconjugated BAs in the intestine are also subjected to deamidation by enterobacteria, especially in the mid to lower ileum and large intestine (Northfield and McColl, 1973;Ridlon et al, 2006). As shown in Table 1, the BA pool in the cecum (vs. liver tissue and gallbladder bile) is dominated by nonamidated LCA (17.5%), DCA (29.5%), CDCA (20.1%), CA (14.8%), and UDCA (3.5%).…”

Ectopic opening of the common bile duct into the stomach

“…The patient's symptoms subsided following biliary diversion (5). However, when pH increases, bile acids can induce gastric mucosal damage (27). It is not clear whether bile damage causes cancer.…”

Aberrant Opening of the Common Bile Duct with Precancerous Change

“…As mentioned above, the second result of the absence of a sphincteric structure in the ectopic biliary opening site is the free bile flux into the duodenal bulb and stomach without control. Bile is very ionic and can lead to mucosal damage by deteriorating the surfactant characteristics of the protective mucous layer [36]. Deformation of the duodenal bulb can develop after chronic exposure to the noxious effects of ionic bile acids and alkaline pH causing mucosal damage and ulceration, which cannot be prevented by cytoprotective mechanisms.…”