Journal articles: 'Bile Acids'

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Kritchevsky, D. "Bile acids." European Journal of Cancer Prevention 1 (October 1991): 23–28. http://dx.doi.org/10.1097/00008469-199110002-00005.

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Patrick, Ping H., and William H. Elliott. "Bile acids." Journal of Chromatography A 347 (January 1985): 155–62. http://dx.doi.org/10.1016/s0021-9673(01)95479-2.

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Abbott, David A., David E. Schlarman, Ping H. Patrick, Daniel M. Tal, and William H. Elliott. "Bile acids." Analytical Biochemistry 146, no. 2 (May 1985): 437–41. http://dx.doi.org/10.1016/0003-2697(85)90566-4.

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Mikov, Momir, and J. Paul Fawcett. "Bile acids." European Journal of Drug Metabolism and Pharmacokinetics 31, no. 3 (September 2006): 133–34. http://dx.doi.org/10.1007/bf03190709.

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KURAMOTO, Taiju, Junko MIYAMOTO, Masaki KONISHI, Takahiko HOSHITA, Takako MASUI, and Mizuho UNE. "Bile Acids in Porcine Fetal Bile." Biological & Pharmaceutical Bulletin 23, no. 10 (2000): 1143–46. http://dx.doi.org/10.1248/bpb.23.1143.

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Paumgartner, Gustav. "Serum bile acids." Journal of Hepatology 2, no. 2 (January 1986): 291–98. http://dx.doi.org/10.1016/s0168-8278(86)80088-5.

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Phillipson, Maggie. "Bile acids revisited." Food and Chemical Toxicology 25, no. 11 (November 1987): 881–82. http://dx.doi.org/10.1016/0278-6915(87)90274-2.

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Hamilton, James P., Guofeng Xie, Jean-Pierre Raufman, Susan Hogan, Terrance L. Griffin, Christine A. Packard, Dale A. Chatfield, Lee R. Hagey, Joseph H. Steinbach, and Alan F. Hofmann. "Human cecal bile acids: concentration and spectrum." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 1 (July 2007): G256—G263. http://dx.doi.org/10.1152/ajpgi.00027.2007.

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To obtain information on the concentration and spectrum of bile acids in human cecal content, samples were obtained from 19 persons who had died an unnatural death from causes such as trauma, homicide, suicide, or drug overdose. Bile acid concentration was measured via an enzymatic assay for 3α-hydroxy bile acids; bile acid classes were determined by electrospray ionization mass spectrometry and individual bile acids by gas chromatography mass spectrometry and liquid chromatography mass spectrometry. The 3α-hydroxy bile acid concentration (μmol bile acid/ml cecal content) was 0.4 ± 0.2 mM (mean ± SD); the total 3-hydroxy bile acid concentration was 0.6 ± 0.3 mM. The aqueous concentration of bile acids (supernatant after centrifugation) was identical, indicating that most bile acids were in solution. By liquid chromatography mass spectrometry, bile acids were mostly in unconjugated form (90 ± 9%, mean ± SD); sulfated, nonamidated bile acids were 7 ± 5%, and nonsulfated amidated bile acids (glycine or taurine conjugates) were 3 ± 7%. By gas chromatography mass spectrometry, 10 bile acids were identified: deoxycholic (34 ± 16%), lithocholic (26 ± 10%), and ursodeoxycholic (6 ± 9), as well as their primary bile acid precursors cholic (6 ± 9%) and chenodeoxycholic acid (7 ± 8%). In addition, 3β-hydroxy derivatives of some or all of these bile acids were present and averaged 27 ± 18% of total bile acids, indicating that 3β-hydroxy bile acids are normal constituents of cecal content. In the human cecum, deconjugation and dehydroxylation of bile acids are nearly complete, resulting in most bile acids being in unconjugated form at submicellar and subsecretory concentrations.

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Das, John B., Nicholas D. Poulos, and G. Ghaus Ansari. "Biliary Lipid Composition and Bile Acid Profiles During and After Enteral Fast of Total Parenteral Nutrition in the Rabbit." Journal of Pediatric Gastroenterology and Nutrition 22, no. 1 (January 1996): 85–91. http://dx.doi.org/10.1002/j.1536-4801.1996.tb01508.x.

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SummaryFeeding and fasting influence biliary lipid composition. With total parenteral nutrition (TPN), it is possible to study the effects of a long‐term “enteral fast” on biliary lipid composition without the metabolic illeffects on nutrient deprivation. We compared the lipid and bile acid (BA) contents of hepatic and gallbladder biles in rabbits on completion of a 14‐day regimen of TPN with those in rabbits returned to oral feeds for 6 weeks after a similar spell of TPN. Chow‐fed rabbits served as controls. With TPN, plasma phospholipid and cholesterol levels were elevated. Basal bile flow and the secretion of bile acids and phospholipids were decreased in the TPN and post‐TPN groups, while the cholesterol secretion rate was essentially unchanged. During TPN, the molar percent of cholesterol (relative to bile acids and phospholipid) in hepatic bile was increased. Biliary glycolithocholic acid (GLCA; as a percent of total conjugated BA) in hepatic bile increased from 1.7% (0.9% SEM) in the chow‐fed to 8.5% (1.5% SEM) during TPN. In TPN and post‐TPN groups, the gallbladder was enlarged to more than twice normal (chow‐fed) size, and contained a dark, mucoid bile (biliary sludge). In this bile, (a) there was a 2.5‐fold increase in bile acid concentration; and (b) the molar percent of cholesterol decreased while that of bile acids increased. TPN produced a state of functional cholestasis, which extended into the post‐TPN period. Gallbladder distension was the common denominator of the hepatobiliary dysfunction in the TPN and post‐TPN rabbits. With sequestration of bile acids in the gallbladder during and after TPN, the circulating bile acid pool was constricted, and the enterohepatic circulation impaired. As cholesterol secretion was low at all times, cholesterol supersaturation did not occur. The molar percent of cholesterol in gallbladder bile decreased, while that of bile acids increased; this suggests absorption of cholesterol by gallbladder mucosa. The increase in biliary GLCA probably resulted from bacterial biotransformation of glycochenodeoxycholic acid to lithocholic acid and its increased absorption from the cecum during TPN.

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Camilleri, Michael. "Bile acid detergency: permeability, inflammation, and effects of sulfation." American Journal of Physiology-Gastrointestinal and Liver Physiology 322, no. 5 (May 1, 2022): G480—G488. http://dx.doi.org/10.1152/ajpgi.00011.2022.

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Bile acids are amphipathic, detergent molecules. The detergent effects of di-α-hydroxy-bile acids are relevant to several colonic diseases. The aims were to review the concentrations of bile acids reaching the human colon in health and disease, the molecular structure of bile acids that determine detergent functions and the relationship to human diseases (neuroendocrine tumors, microscopic colitis, active celiac disease, and ulcerative colitis, Crohn’s disease and ileal resection), the relationship to bacterial uptake into the mucosa, mucin depletion, and epithelial damage, the role of bile acids in mucosal inflammation and microscopic colitis, and the role of sulfation of bile salts in detoxification or prevention of the detergent effects of bile acids. The concentrations of bile acids reaching the human colon range from 2 to 10 mM; di-α-hydroxy bile acids are the only bile acids with detergent effects that include mucin depletion, mucosal damage, bacterial uptake, and microscopic inflammation that may be manifest in diseases associated with no overt inflammation of the mucosa, such as bile acid diarrhea, ileal diseases such as neuroendocrine tumors, ileal resection, and nonalcoholic steatohepatitis. Sulfation inactivates colonic secretion due to primary bile acids, but it may render secondary bile acids proinflammatory in the colon. Other evidence in preclinical models of inflammatory bowel disease (IBD) suggests reduced sulfation causes barrier dysfunction, inflammation, or carcinogenesis. These advances emphasize relevance and opportunities afforded by greater understanding of the chemistry and metabolism of bile acids, which stands to be further enhanced by research into the metabolic interactions of microbiota with bile acids.

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Camogliano, L., and A. Casu. "Bile acids in bile after monensin treatment." Experimental pathology 36, no. 1 (January 1989): 37–41. http://dx.doi.org/10.1016/s0232-1513(89)80108-2.

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Shulpekova, Yulia, Elena Shirokova, Maria Zharkova, Pyotr Tkachenko, Igor Tikhonov, Alexander Stepanov, Alexandra Synitsyna, et al. "A Recent Ten-Year Perspective: Bile Acid Metabolism and Signaling." Molecules 27, no. 6 (March 18, 2022): 1983. http://dx.doi.org/10.3390/molecules27061983.

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Bile acids are important physiological agents required for the absorption, distribution, metabolism, and excretion of nutrients. In addition, bile acids act as sensors of intestinal contents, which are determined by the change in the spectrum of bile acids during microbial transformation, as well as by gradual intestinal absorption. Entering the liver through the portal vein, bile acids regulate the activity of nuclear receptors, modify metabolic processes and the rate of formation of new bile acids from cholesterol, and also, in all likelihood, can significantly affect the detoxification of xenobiotics. Bile acids not absorbed by the liver can interact with a variety of cellular recipes in extrahepatic tissues. This provides review information on the synthesis of bile acids in various parts of the digestive tract, its regulation, and the physiological role of bile acids. Moreover, the present study describes the involvement of bile acids in micelle formation, the mechanism of intestinal absorption, and the influence of the intestinal microbiota on this process.

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Amelsberg, Andree, Christina Jochims, Claus Peter Richter, Rolf Nitsche, and Ulrich R. Fölsch. "Evidence for an anion exchange mechanism for uptake of conjugated bile acid from the rat jejunum." American Journal of Physiology-Gastrointestinal and Liver Physiology 276, no. 3 (March 1, 1999): G737—G742. http://dx.doi.org/10.1152/ajpgi.1999.276.3.g737.

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Absorption of conjugated bile acids from the small intestine is very efficient. The mechanisms of jejunal absorption are not very well understood. The aim of this study was to clarify the mechanism of absorption of conjugated bile acid at the apical membrane of jejunal epithelial cells. Brush-border membrane vesicles from intestinal epithelial cells of the rat were prepared. Absorption of two taurine-conjugated bile acids that are representative of endogenous bile acids in many variate vertebrate species were studied. In ileal, but not jejunal brush-border membrane vesicles, transport of conjugated bile acids was cis-stimulated by sodium. Transport of conjugated bile acids was trans-stimulated by bicarbonate in the jejunum. Absorption of conjugated dihydroxy-bile acids was almost twice as fast as of trihydroxy-bile acids. Coincubation with other conjugated bile acids, bromosulfophthalein, and DIDS, as well as by incubation in the cold inhibited the transport rate effectively. Absorption of conjugated bile acids in the jejunum from the rat is driven by anion exchange and is most likely an antiport transport.

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Obinata, K., H. Nittono, K. Yabuta, R. Mahara, and M. Tohma. "1β‐Hydroxylated Bile Acids in the Urine of Healthy Neonates." Journal of Pediatric Gastroenterology and Nutrition 15, no. 1 (July 1992): 1–5. http://dx.doi.org/10.1002/j.1536-4801.1992.tb10594.x.

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SummaryIn order to clarify the metabolism of bile acids in neonates, 1β‐hydroxylated bile acids in the urine of healthy newborns were examined by gas chromatogra‐phy‐mass spectrometry. The results showed that the percentage of total lβ‐hydroxylated bile acids, 3β,12a‐dihydroxy‐5‐cholenoic acid and hyocholic acid in neonates was significantly higher than in older children. The ratio of lβ‐hydroxylated bile acids to their comparable primary bile acids was also higher in neonates than in older children. These results suggest that 1β‐ and 6α‐hydroxylation of bile acids are the predominant pathways of bile acid metabolism in neonates.

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Madsen, Karen. "Intestinal Absorption of Bile Salts." Canadian Journal of Gastroenterology 4, no. 2 (1990): 79–84. http://dx.doi.org/10.1155/1990/624985.

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Bile acids are secreted from the liver into the duodenum where they aid in the digestion and absorption of dietary lipids. Absorption of bile acids occurs through both ionic and nonionic diffusion in the jejunum and colon and through an active sodium ion-dependent carrier mechanism in the ileum. The prima, y bile acids synthesized in the liver can be converted by intestinal bacteria into secondary and tertiary bile acids. Bile acids may also be conjugated with glycine or taurine which results in an increase in the hydrophilicity and solubility of these compounds at physiological pH. The amount of passive diffusion of bile acids that occurs across the brush border membrane along the length of the entire intestine depends upon the ratio of ionized to nonionized bile acids coupled with the bile salt concentration and the individual permeability coefficients of monomers. Active transport of both conjugated and nonconjugated species of bile acids depends upon the presence of a single negative charge on the side chain. Maximal transport rates for bile acids are related to the number of hydroxyl groups present while the Michaelis-Menten constant for transport is dependent upon whether or not the bile acid is conjugated. Although active uptake of bile acids from the ileum has been considered the major route for bile salt absorption in the small intestine, the mechanism may actually be responsible for only a small proportion of the total bile acid pool absorbed from the lumen.

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Trefflich, Iris, Hanns-Ulrich Marschall, Romina di Giuseppe, Marcus Ståhlman, Andreas Michalsen, Alfonso Lampen, Klaus Abraham, and Cornelia Weikert. "Associations between Dietary Patterns and Bile Acids—Results from a Cross-Sectional Study in Vegans and Omnivores." Nutrients 12, no. 1 (December 23, 2019): 47. http://dx.doi.org/10.3390/nu12010047.

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Bile acids play an active role in fat metabolism and, in high-fat diets, elevated concentrations of fecal bile acids may be related to an increased risk of colorectal cancer. This study investigated concentrations of fecal and serum bile acids in 36 vegans and 36 omnivores. The reduced rank regression was used to identify dietary patterns associated with fecal bile acids. Dietary patterns were derived with secondary and conjugated fecal bile acids as response variables and 53 food groups as predictors. Vegans had higher fiber (p < 0.01) and lower fat (p = 0.0024) intake than omnivores. In serum, primary and glycine-conjugated bile acids were higher in vegans than in omnivores (p ≤ 0.01). All fecal bile acids were significantly lower in vegans compared to omnivores (p < 0.01). Processed meat, fried potatoes, fish, margarine, and coffee contributed most positively, whereas muesli most negatively to a dietary pattern that was directly associated with all fecal bile acids. According to the pattern, fat intake was positively and fiber intake was inversely correlated with bile acids. The findings contribute to the evidence that, in particular, animal products and fat may play a part in higher levels of fecal bile acids.

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Camilleri, Michael, and Gregory J. Gores. "Therapeutic targeting of bile acids." American Journal of Physiology-Gastrointestinal and Liver Physiology 309, no. 4 (August 15, 2015): G209—G215. http://dx.doi.org/10.1152/ajpgi.00121.2015.

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The first objectives of this article are to review the structure, chemistry, and physiology of bile acids and the types of bile acid malabsorption observed in clinical practice. The second major theme addresses the classical or known properties of bile acids, such as the role of bile acid sequestration in the treatment of hyperlipidemia; the use of ursodeoxycholic acid in therapeutics, from traditional oriental medicine to being, until recently, the drug of choice in cholestatic liver diseases; and the potential for normalizing diverse bowel dysfunctions in irritable bowel syndrome, either by sequestering intraluminal bile acids for diarrhea or by delivering more bile acids to the colon to relieve constipation. The final objective addresses novel concepts and therapeutic opportunities such as the interaction of bile acids and the microbiome to control colonic infections, as in Clostridium difficile-associated colitis, and bile acid targeting of the farnesoid X receptor and G protein-coupled bile acid receptor 1 with consequent effects on energy expenditure, fat metabolism, and glycemic control.

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Shansky, Yaroslav, and Julia Bespyatykh. "Bile Acids: Physiological Activity and Perspectives of Using in Clinical and Laboratory Diagnostics." Molecules 27, no. 22 (November 13, 2022): 7830. http://dx.doi.org/10.3390/molecules27227830.

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Bile acids play a significant role in the digestion of nutrients. In addition, bile acids perform a signaling function through their blood-circulating fraction. They regulate the activity of nuclear and membrane receptors, located in many tissues. The gut microbiota is an important factor influencing the effects of bile acids via enzymatic modification. Depending on the rate of healthy and pathogenic microbiota, a number of bile acids may support lipid and glucose homeostasis as well as shift to more toxic compounds participating in many pathological conditions. Thus, bile acids can be possible biomarkers of human pathology. However, the chemical structure of bile acids is similar and their analysis requires sensitive and specific methods of analysis. In this review, we provide information on the chemical structure and the biosynthesis of bile acids, their regulation, and their physiological role. In addition, the review describes the involvement of bile acids in various diseases of the digestive system, the approaches and challenges in the analysis of bile acids, and the prospects of their use in omics technologies.

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Hild, Benedikt, Hauke S. Heinzow, Hartmut H. Schmidt, and Miriam Maschmeier. "Bile Acids in Control of the Gut-Liver-Axis." Zeitschrift für Gastroenterologie 59, no. 01 (January 2021): 63–68. http://dx.doi.org/10.1055/a-1330-9644.

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AbstractThe liver and gut share an intimate relationship whose communication relies heavily on metabolites, among which bile acids play a major role. Beyond their function as emulsifiers, bile acids have been recognized for their influence on metabolism of glucose and lipids as well as for their impact on immune responses. Therefore, changes to the composition of the bile acid pool can be consequential to liver and to gut physiology. By metabolizing primary bile acids to secondary bile acids, the bacterial gut microbiome modifies how bile acids exert influence. An altered ratio of secondary to primary bile acids is found to be substantial in many studies. Thus, disease pathogenesis and progression could be changed by gut microbiome modification which influences the bile acid pool.

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Jönsson, Gerd, Ann‐Christine Midtvedt, Arne Norman, and Tore Midtvedt. "Intestinal Microbial Bile Acid Transformation in Healthy Infants." Journal of Pediatric Gastroenterology and Nutrition 20, no. 4 (May 1995): 394–402. http://dx.doi.org/10.1002/j.1536-4801.1995.tb11578.x.

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Summary: Following the establishment of functionally active intestinal flora in three healthy Swedish children from birth up to 24 months of age, we investigated the development of different 24‐carbon bile acids. The fecal bile acids were group‐separated into unconjugated, glycine‐conjugated, taurine‐conjugated, and sulfated, so that we could follow the changes between the different fractions of conjugates. In meconium, most (55–63%) of the bile acids were conjugated with taurine; only 11–32% were conjugated with glycine. Deconjugation was the first sign of intestinal microbial activity on the bile acids. Already at 1 month of age, most of the bile acids were deconjugated; among the conjugated bile acids, the glycine‐conjugated dominated over the taurine‐conjugated. An unidentified conjugate of cholic and chenodeoxycholic acids (C, CDC) that separated with the sulfated bile acids was found. The unconjugated bile acids and those that arose from hydrolysis of existing conjugates were separated and identified by gas‐liquid chromatography coupled to mass spectrometry (GC‐MS). Twenty‐nine different bile acids were identified. In meconium, 16 different bile acids were identified. C and CDC were identified in all samples. The bile acid pattern changed during the course of the study. Many of the identified bile acids were only found in one or a few of the analyzed samples, and sometimes only in samples from one child. 6α‐hydroxylated bile acids, probably not microbially synthesized, were present at high percentages in the children. Child 2 was the first, at 6 months of age, to establish microbes with 7α‐dehydroxylase activity; at 24 months of age, the establishment was almost complete in all three children. At each sampling age, there was at least one sample containing bile acids with one or two hydroxyl groups that had been oxidized to oxo‐, or further reduced to a hydroxyl group in the p‐position. The sum of these metabolites varied between 0 and 26%, and no significant difference was found between meconium and the samples at 24 months of age.

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IIDA, Takashi, Toshiaki MOMOSE, Frederic C. CHANG, Junichi GOTO, and Tosio NAMBARA. "Potential bile acid metabolites. XV. Synthesis of 4.BETA.-hydroxylated bile acids; unique bile acids in human fetal bile." CHEMICAL & PHARMACEUTICAL BULLETIN 37, no. 12 (1989): 3323–29. http://dx.doi.org/10.1248/cpb.37.3323.

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Gómez, Cristina, Simon Stücheli, Denise V. Kratschmar, Jamal Bouitbir, and Alex Odermatt. "Development and Validation of a Highly Sensitive LC-MS/MS Method for the Analysis of Bile Acids in Serum, Plasma, and Liver Tissue Samples." Metabolites 10, no. 7 (July 9, 2020): 282. http://dx.doi.org/10.3390/metabo10070282.

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Bile acids control lipid homeostasis by regulating uptake from food and excretion. Additionally, bile acids are bioactive molecules acting through receptors and modulating various physiological processes. Impaired bile acid homeostasis is associated with several diseases and drug-induced liver injury. Individual bile acids may serve as disease and drug toxicity biomarkers, with a great demand for improved bile acid quantification methods. We developed, optimized, and validated an LC-MS/MS method for quantification of 36 bile acids in serum, plasma, and liver tissue samples. The simultaneous quantification of important free and taurine- and glycine-conjugated bile acids of human and rodent species has been achieved using a simple workflow. The method was applied to a mouse model of statin-induced myotoxicity to assess a possible role of bile acids. Treatment of mice for three weeks with 5, 10, and 25 mg/kg/d simvastatin, causing adverse skeletal muscle effects, did not alter plasma and liver tissue bile acid profiles, indicating that bile acids are not involved in statin-induced myotoxicity. In conclusion, the established LC-MS/MS method enables uncomplicated sample preparation and quantification of key bile acids in serum, plasma, and liver tissue of human and rodent species to facilitate future studies of disease mechanisms and drug-induced liver injury.

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Popova, O. S., and L. A. Agafonova. "Features of bile acid metabolism in fish." International Journal of Veterinary Medicine, no. 1 (April 27, 2022): 61–65. http://dx.doi.org/10.52419/issn2072-2419.2022.1.61.

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The fish liver is an important organ involved in the complex metabolism of bile and bile acids. The biochemical reactions that occur during this process directly depend on the functional state of the digestive system and fish nutrition. Knowledge of the features of bile acid metabolism will allow designing the cheapest and at the same time effective drugs for the pharmacological correction of hepatopathy. The composition of bile acids depends on the type of food, so in fish such as pike, perch, carp, cholic and deoxycholic acids conjugated with taurine are more common. In predatory fish, cholic acid predominates, in contrast to benthivorous fish. Substances secreted with bile do not participate in the general metabolism of tissues, so that hepatocytes do not need to constantly secrete large volumes of bile.The metabolism of bile acids is carried out by the liver and is called the enterohepatic circulation. It all starts with the biological precursor of bile acids - cholesterol. Cholesterol in the body is formed during the absorption of lipids in the intestine. Two-thirds of exogenous cholesterol is excreted from the body in the form of bile acids. As a result of transformation by hepatocytes, primary bile acids are formed - cholic and chenodioxycholic. Then they are cojugated with taurine or glycine in the C-24 region of the carboxyl group and are excreted from hepatocytes continuously through the bile ducts to the gallbladder and further to the intestine. In the intestine, under the influence of microbial metabolites, they are hydroxylated and converted into secondary bile acids. Cholic becomes deoxycholic, and chenodisoxycholic becomes lithocholic. A small amount of bile acids are in a free state and form paired compounds. 90% of bile acids in the intestine form complexes of choleic acids in combination with fatty acids, which are absorbed through the wall of enterocytes. In enterocytes, these complexes again disintegrate and bile acids again enter the liver through the portal vein. Thus the circle of metabolism is closed.

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Majait, Soumia, Max Nieuwdorp, Marleen Kemper, and Maarten Soeters. "The Black Box Orchestra of Gut Bacteria and Bile Acids: Who Is the Conductor?" International Journal of Molecular Sciences 24, no. 3 (January 17, 2023): 1816. http://dx.doi.org/10.3390/ijms24031816.

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Over the past decades the potential role of the gut microbiome and bile acids in type 2 diabetes mellitus (T2DM) has been revealed, with a special reference to low bacterial alpha diversity. Certain bile acid effects on gut bacteria concern cytotoxicity, or in the case of the microbiome, bacteriotoxicity. Reciprocally, the gut microbiome plays a key role in regulating the bile acid pool by influencing the conversion and (de)conjugation of primary bile acids into secondary bile acids. Three main groups of bacterial enzymes responsible for the conversion of bile acids are bile salt hydrolases (BSHs), hydroxysteroid dehydrogenases (HSDHs) and enzymes encoded in the bile acid inducible (Bai) operon genes. Interventions such as probiotics, antibiotics and fecal microbiome transplantation can impact bile acids levels. Further evidence of the reciprocal interaction between gut microbiota and bile acids comes from a multitude of nutritional interventions including macronutrients, fibers, prebiotics, specific individual products or diets. Finally, anatomical changes after bariatric surgery are important because of their metabolic effects. The heterogeneity of studies, diseases, bacterial species and (epi)genetic influences such as nutrition may challenge establishing specific and detailed interventions that aim to tackle the gut microbiome and bile acids.

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LaFleur, Bonnie, Weiqun Tong, Junmei Liu, M. Peter Lance, and Patricia Thompson. "Determinants of bile acids." Journal of Clinical Oncology 30, no. 4_suppl (February 1, 2012): 632. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.632.

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632 Background: Several epidemiological studies have demonstrated an association between bile acids (BA) and colorectal cancer. Despite this evidence, there are limited studies that examine the determinants of bile acids in humans. We conducted a secondary, cross-sectional analysis on 735 adenoma formers from a phase III adenoma prevention trial of ursodeoxycholic acid (URSO) who provided a fecal sample at their baseline visit. Methods: Fecal measures of primary bile acids cholic acid (CA) and chenodoxycholic acid (CDCA), as well as secondary bile acids, deoxycholic acid (DCA), lithocholic (LCA) were the outcome variables of interest. Dietary, non-dietary, medication use, genetic variation in the CYP7A1 gene (as single nucleotide polymorphisms (SNPs) and haplotypes), and physical activity, and characteristics of baseline adenoma were evaluated as correlates of fecal BAs. We used maximum likelihood methods to incorporate left-censoring in the BAs that had concentrations below the detection limit (BDL). These log-normal parametric survival models were used to fit potential predictors of fecal BA levels, stratifying by sex. The Akaike information criterion (AIC) was used to choose the best predictive model from each BA outcome. Model accuracy was assessed using leave-one-out cross validation and a likelihood-based measure of R2 and the Brier score. Results: LDL and cholesterol were predictors for primary bile acid CDCA in men and women, as was the use of pain medication (use of medication lowered BA levels). Genetic variation in CYP7A1 (as haplotypes and individual SNP's) was a significant determinant of CA level in both men and women. BMI was an important predictor for both men and women for DCA and CA. Presentation with tubular-villous histology was associated with LCA levels whereas proximal adenoma was an important predictor for CA levels, in men and women. Conclusions: This secondary analysis of a uniquely large dataset validates previous studies that suggest lifestyle and genetic factors influence colonic exposure to carcinogenic BAs. These findings also importantly highlight gender-specific differences in BA determinants that may explain colorectal cancer incidence differences between men and women.

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Makin, H. L. J. "Sterols and bile acids." Gut 27, no. 10 (October 1, 1986): 1232–33. http://dx.doi.org/10.1136/gut.27.10.1232-b.

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Leveille-Webster, Cynthia. "Bile acids—What's new." Clinical Techniques in Small Animal Practice 12, no. 1 (February 1997): 2–9. http://dx.doi.org/10.1016/s1096-2867(97)80038-2.

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McIlvride, Saraid, Peter H. Dixon, and Catherine Williamson. "Bile acids and gestation." Molecular Aspects of Medicine 56 (August 2017): 90–100. http://dx.doi.org/10.1016/j.mam.2017.05.003.

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Reuben, Adrian. "Sterols and bile acids." Gastroenterology 93, no. 1 (July 1987): 214–15. http://dx.doi.org/10.1016/0016-5085(87)90349-0.

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Azerad, R. "Sterols and bile acids." Biochimie 69, no. 5 (May 1987): 555–56. http://dx.doi.org/10.1016/0300-9084(87)90096-4.

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Dempsey, Laurie A. "Bile acids block NLRP3." Nature Immunology 17, no. 11 (October 19, 2016): 1243. http://dx.doi.org/10.1038/ni.3597.

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Out, Carolien, Folkert Kuipers, and Albert K. Groen. "Bile Acids and Cholestasis." Gastroenterology 144, no. 2 (February 2013): e17-e18. http://dx.doi.org/10.1053/j.gastro.2012.10.053.

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Karpen, Saul J. "Bile acids go nuclear!" Hepatology 30, no. 4 (October 1999): 1107–9. http://dx.doi.org/10.1002/hep.510300439.

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KANDA, Tatsuo, Laurent FOUCAND, Yuichi NAKAMURA, Isabelle NIOT, Philippe BESNARD, Michiyo FUJITA, Yasuo SAKAI, Katsuyoshi HATAKEYAMA, Teruo ONO, and Hiroshi FUJII. "Regulation of expression of human intestinal bile acid-binding protein in Caco-2 cells." Biochemical Journal 330, no. 1 (February 15, 1998): 261–65. http://dx.doi.org/10.1042/bj3300261.

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Molecular mechanisms of the bile acid active transport system in the ileal enterocytes remain unknown. We examined whether bile acids affect human enterocyte gene expression of intestinal bile acid-binding protein (I-BABP), a component of this transport system. Differentiated Caco-2 cells were incubated in the presence of human bile, bile acids or other lipids. The level of I-BABP expression was evaluated by Northern and Western blot analyses. A 24 h incubation of Caco-2 cells in a medium containing either bile or bile acids resulted in a remarkable 7.5-fold increase in the I-BABP mRNA level over the control level. Neither cholesterol, palmitic acid, phosphatidylcholine nor cholestyramine treated bile showed any difference in I-BABP mRNA expression from the control. Bile acid treatment increased the level of I-BABP mRNA in Caco-2 cells in a time- and dose-dependent manner. Western blot analysis showed that this induction led to increase in cytosolic I-BABP. Chenodeoxycholic acid and deoxycholic acid showed greater induction effects than other hydrophilic bile acids, including their own glycine conjugates. Pretreatment by actinomycin D or cycloheximide completely inhibited the up-regulation of I-BABP expression by bile acid. Bile acids, especially lipophilic bile acids, increase the I-BABP expression in Caco-2-cells, suggesting that luminal bile acids play an important role in regulating the I-BABP gene expression.

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Soroka, Carol J., Heino Velazquez, Albert Mennone, Nazzareno Ballatori, and James L. Boyer. "Ostα depletion protects liver from oral bile acid load." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 3 (September 2011): G574—G579. http://dx.doi.org/10.1152/ajpgi.00141.2011.

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Bile acid homeostasis is tightly maintained through interactions between the liver, intestine, and kidney. During cholestasis, the liver is incapable of properly clearing bile acids from the circulation, and alternative excretory pathways are utilized. In obstructive cholestasis, urinary elimination is often increased, and this pathway is further enhanced after bile duct ligation in mice that are genetically deficient in the heteromeric, basolateral organic solute transporter alpha-beta (Ostα-Ostβ). In this study, we examined renal and intestinal function in Ostα-deficient and wild-type mice in a model of bile acid overload. After 1% cholic acid feeding, Ostα-deficient mice had significantly lower serum ALT levels compared with wild-type controls, indicating partial protection from liver injury. Urinary clearance of bile acids, but not clearance of [3H]inulin, was significantly higher in cholic acid-fed Ostα-deficient mice compared with wild-type mice but was not sufficient to account for the protection. Fecal excretion of bile acids over the 5 days of cholic acid feeding was responsible for almost all of the bile acid loss in Ostα-deficient mice, suggesting that intestinal losses of bile acids accounted for the protection from liver injury. Thus fecal loss of bile acids after bile acid overload reduced the need for the kidney to filter and excrete the excess bile acids. In conclusion, Ostα-deficient mice efficiently eliminate excess bile acids via the feces. Inhibition of intestinal bile acid absorption might be an effective therapeutic target in early stages of cholestasis when bile acids are still excreted into bile.

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Abu-Hayyeh, Shadi, Georgia Papacleovoulou, and Catherine Williamson. "Nuclear receptors, bile acids and cholesterol homeostasis series – Bile acids and pregnancy." Molecular and Cellular Endocrinology 368, no. 1-2 (April 2013): 120–28. http://dx.doi.org/10.1016/j.mce.2012.10.027.

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Hagi, Tatsuro, Sharon Y. Geerlings, Bart Nijsse, and Clara Belzer. "The effect of bile acids on the growth and global gene expression profiles in Akkermansia muciniphila." Applied Microbiology and Biotechnology 104, no. 24 (November 7, 2020): 10641–53. http://dx.doi.org/10.1007/s00253-020-10976-3.

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Abstract Akkermansia muciniphila is a prominent member of the gut microbiota and the organism gets exposed to bile acids within this niche. Several gut bacteria have bile response genes to metabolize bile acids or an ability to change their membrane structure to prevent membrane damage from bile acids. To understand the response to bile acids and how A. muciniphila can persist in the gut, we studied the effect of bile acids and individual bile salts on growth. In addition, the change in gene expression under ox-bile condition was studied. The growth of A. muciniphila was inhibited by ox-bile and the bile salts mixture. Individual bile salts have differential effects on the growth. Although most bile salts inhibited the growth of A. muciniphila, an increased growth was observed under culture conditions with sodium deoxycholate. Zaragozic acid A, which is a squalene synthase inhibitor leading to changes in the membrane structure, increased the susceptibility of A. muciniphila to bile acids. Transcriptome analysis showed that gene clusters associated with an ABC transporter and RND transporter were upregulated in the presence of ox-bile. In contrast, a gene cluster containing a potassium transporter was downregulated. Membrane transporter inhibitors also decreased the tolerance to bile acids of A. muciniphila. Our results indicated that membrane transporters and the squalene-associated membrane structure could be major bile response systems required for bile tolerance in A. muciniphila. Key points • The growth of Akkermansia muciniphila was inhibited by most bile salts. • Sodium deoxycholate increased the growth of A. muciniphila. • The genes encoding transporters and hopanoid synthesis were upregulated by ox-bile. • The inhibitors of transporters and hopanoid synthesis reduced ox-bile tolerance.

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Wolkoff, Allan W., and David E. Cohen. "I. Hepatocyte transport of bile acids." American Journal of Physiology-Gastrointestinal and Liver Physiology 284, no. 2 (February 1, 2003): G175—G179. http://dx.doi.org/10.1152/ajpgi.00409.2002.

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Bile acids are cholesterol derivatives that serve as detergents in bile and the small intestine. Approximately 95% of bile acids secreted by hepatocytes into bile are absorbed from the distal ileum into the portal venous system. Extraction from the portal circulation by the hepatocyte followed by reexcretion into the bile canaliculus completes the enterohepatic circulation of these compounds. Over the past few years, candidate bile acid transport proteins of the sinusoidal and canalicular plasma membranes of the hepatocyte have been identified. The physiology of hepatocyte bile acid transport and its relationship to these transport proteins is the subject of this Themes article.

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Muto, Yamato, Mitsuyoshi Suzuki, Genta Kakiyama, Takahiro Sasaki, Tsuyoshi Murai, Hajime Takei, and Hiroshi Nittono. "Profiling of Urinary Glucuronidated Bile Acids across Age Groups." Metabolites 12, no. 12 (December 7, 2022): 1230. http://dx.doi.org/10.3390/metabo12121230.

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We investigated the age-dependent changes in urinary excretion of glucuronidated bile acids at the C-3 position. Bile acid 3-glucuronides accounted for 0.5% of urinary bile acids in neonates, and the proportion of bile acid 3-glucuronides plateaued at 1–3 years of age. The 3-glucuronides of secondary bile acids were first secreted at 3 months of age, the same time as the establishment of the gut bacterial flora in infants. A considerable portion of bile acid 3-glucuronides were present as non-amidated forms. Our results indicate dynamic hepatic enzyme activity in which the levels of uridine 5′-diphospho-glucuronosyltransferases (UGTs) differ by age group, with higher glucuronidation activity of UGTs towards nonamidated bile acids than amidated bile acids.

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An, Chihyeok, Hyeyeon Chon, Wanrim Ku, Sunho Eom, Mingyu Seok, Sangha Kim, Jaesun Lee, et al. "Bile Acids: Major Regulator of the Gut Microbiome." Microorganisms 10, no. 9 (September 6, 2022): 1792. http://dx.doi.org/10.3390/microorganisms10091792.

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Bile acids are synthesized from cholesterol and play an important role in regulating intestinal microflora. The different degrees of hydrophobicity and acidity of individual bile acids may affect their antimicrobial properties. We examined the antimicrobial effects of different bile acids on various microorganisms in vitro and confirmed whether these remain consistent in vivo. Using human bile acids, including ursodeoxycholic acid, cholic acid, chenodeoxycholic acid, deoxycholic acid, and lithocholic acid, a disc diffusion test was performed, and a rodent model was created to determine the antimicrobial effects of each bile acid. The fecal bacterial population was analyzed using a real-time polymerase chain reaction. Each bile acid showed different microbial inhibitory properties. The inhibitory activity of bile acids against microbiota which normally resides in the gastrointestinal tract and biliary system, was low; however, normal flora of other organs was significantly inhibited. Changes in microbial counts after bile acid administration in a rodent model differed in the colon and cecum. The in vivo and in vitro results show that the antimicrobial effects of bile acids against intestinal microbiota were similar. In conclusion, bile acids could be a novel treatment strategy to regulate gut microbiota.

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Chitranukroh, A., G. Taggart, and B. H. Billing. "Enhancement of the Urinary Excretion of Non-Sulphated and Sulphated Radioactive Bile Acids by Sodium Acetate in the Bile Duct Obstructed Rat." Clinical Science 68, no. 1 (January 1, 1985): 63–70. http://dx.doi.org/10.1042/cs0680063.

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1. The renal clearances of [14C]glycocholate, [14C]taurocholate and [3H]glycochenodeoxycholate-3-sulphate were determined in bile duct obstructed rats. 2. Comparisons of the bile acid clearances with glomerular filtration rates (GFR) indicate that most of the filtered bile acids are reabsorbed. 3. Inhibition studies with p-aminohippurate (PAH) and probenecid suggest that a proportion of the bile acids in urine is secreted. 4. Attempts were made to increase the renal clearance of the bile acids by the administration of pharmacological agents. 5. An infusion of sodium acetate (0.3 mol/l) increased the clearance of the radioactive bile acids and augmented the urinary excretion of endogenous 3α-hydroxy bile acids and reduced their concentration in plasma.

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Jones, M. L., C. Martoni, H. Chen, W. Ouyang, T. Metz, and S. Prakash. "Deconjugation of Bile Acids with Immobilized Genetically EngineeredLactobacillus plantarum80(pCBH1)." Applied Bionics and Biomechanics 2, no. 1 (2005): 31–38. http://dx.doi.org/10.1155/2005/380659.

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Bile acids are important to normal human physiology. However, bile acids can be toxic when produced in pathologically high concentrations in hepatobileary and other diseases. This study shows that immobilized genetically engineeredLactobacillus plantarum80 (pCBH1) (LP80 (pCBH1)) can efficiently hydrolyze bile acids and establishes a basis for their use. Results show that immobilized LP80 (pCBH1) is able to effectively break down the conjugated bile acids into glycodeoxycholic acid (GDCA) and taurodeoxycholic acid (TDCA) with bile salt hydrolase (BSH) activities of 0.17 and 0.07 μmol DCA/mg CDW/h, respectively. The deconjugation product, deoxycholic acid (DCA), was diminished by LP80 (pCBH1) within 4 h of initial BSH activity. Thisin-vitrostudy suggests that immobilized genetically engineered bacterial cells have important potential for deconjugation of bile acids for lowering of high levels of bile acids for therapy.

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Mikov, Momir, Ksenija Kuhajda, and Julijan Kandrac. "Current aspects of pharmacologic application of bile acids." Medical review 56, no. 5-6 (2003): 237–42. http://dx.doi.org/10.2298/mpns0306237m.

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Effects of bile acids and their salts on absorption of other substances Bile acids and their salts increase intestinal absorption of lipids and transmembrane and paracellular transfer of small and endogenous and exogenous polar molecules. It has been established that they are good promotores of insulin absorption through skin and nasal mucose, and of blood-brain barrier transfer of salycilates and quinine. Effects of bile acids and their salts on absorption of other substances and their potential action It has been established that combination of bile acids with amphotericin B has potential Leishmanicideal effect and combination with ciprofloxacine has improved its antibacterial activity against Pseudomonas aeruginosa in vitro. Bile acids pharmacodynamic effects Bile acids have analgesic and hypoglycemic effect They also have anti-HIV effect probably suppressing virus transmission from cell to cell. Conclusion New studies of natural bile acids and new synthetic bile acids have revealed that they are not only adjuvants to existing active principles in pharmaceutical forms, but they can act as new therapeutic agents. However, it is necessary to study their possible mechanisms, but they are not crucial for their therapeutic application. Toxicological and pharmacological studies will determine the role of newly synthetized bile acids and their salts in current therapy.

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POWELL, Ashley A., Janna M. LaRUE, A. K. BATTA, and Jesse D. MARTINEZ. "Bile acid hydrophobicity is correlated with induction of apoptosis and/or growth arrest in HCT116 cells." Biochemical Journal 356, no. 2 (May 24, 2001): 481–86. http://dx.doi.org/10.1042/bj3560481.

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Faecal bile acids have long been associated with colon cancer; highly hydrophobic bile acids, which induce apoptosis, have been implicated in the promotion of colon tumours. The moderately hydrophobic chemopreventive agent ursodeoxycholic acid (UDCA) does not induce apoptosis; rather, it causes colon-derived tumour cells to arrest their growth. To investigate the relationship between bile acid hydrophobicity and biological activity we examined 26 bile acids for their capacity to induce apoptosis or alter cell growth. We found that the rapidity with which, and the degree to which, bile acids could induce apoptosis or growth arrest was correlated with their relative hydrophobicities. Of the bile acids tested, only deoxycholic acid (DCA) and chenodeoxycholic acid, the most hydrophobic bile acids tested, could induce apoptosis in less than 12h in the human colon cancer cell line HCT116. The moderately hydrophobic bile acids hyoDCA, lagoDCA, norDCA, homoUDCA and isoUDCA induced growth arrest at 12h but longer incubations resulted in apoptosis. Conjugation of glycine or taurine to the bile acids decreased relative hydrophobicity and eliminated biological activity in our assays. In addition, we tested a subset of these bile acids for their ability to translocate across cell membranes. When 14C-labelled and 3H-labelled DCA, UDCA and lagoDCA were added to cell cultures, we found only minimal uptake by colon cells, whereas hepatocytes had considerably higher absorption. These experiments suggest that hydrophobicity is an important determinant of the biological activity exhibited by bile acids but that under our conditions these activities are not correlated with cellular uptake.

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Yde, Jonathan, Qi Wu, Johan F. Borg, Robert A. Fenton, and Hanne B. Moeller. "A systems-level analysis of bile acids effects on rat colon epithelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 322, no. 1 (January 1, 2022): G34—G48. http://dx.doi.org/10.1152/ajpgi.00178.2021.

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Feeding rats with a bile acid caused changes in fecal output, underlining this bile acid diarrhea model’s usefulness. Colonic epithelial expression of genes associated with facilitated transport of bile acids was altered during bile acid feeding. The study raises the possibility of regulated colonic transepithelial transport of bile acids in response to luminal bile acids. In addition, this study provides annotated rat colonic epithelial cell transcriptome and proteome with response to bile acid feeding.

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Anwer, Mohammad Sawkat. "Intracellular Signaling by Bile Acids." Journal of Bio-Science 20 (January 13, 2014): 1–23. http://dx.doi.org/10.3329/jbs.v20i0.17647.

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Bile acids, synthesized from cholesterol, are known to produce beneficial as well as toxic effects in the liver. The beneficial effects include choleresis, immunomodulation, cell survival, while the toxic effects include cholestasis, apoptosis and cellular toxicity. It is believed that bile acids produce many of these effects by activating intracellular signaling pathways. However, it has been a challenge to relate intracellular signaling to specific and at times opposing effects of bile acids. It is becoming evident that bile acids produce different effects by activating different isoforms of phosphoinositide 3-kinase (PI3K), Protein kinase Cs (PKCs), and mitogen activated protein kinases (MAPK). Thus, the apoptotic effect of bile acids may be mediated via PI3K-110?, while cytoprotection induce by cAMP-GEF pathway involves activation of PI3K-p110?/? isoforms. Atypical PKC? may mediate beneficial effects and nPKC? may mediate toxic effects, while cPKC? and nPKC? may be involved in both beneficial and toxic effects of bile acids.The opposing effects of nPKC? activation may depend on nPKC? phosphorylation site(s). Activation of ERK1/2 and JNK1/2 pathway appears to mediate beneficial and toxic effects, respectively,of bile acids. Activation of p38? MAPK and p38? MAPK may mediate choleretic and cholestatic effects, respectively, of bile acids. Future studies clarifying the isoform specific effects on bile formation should allow us to define potential therapeutic targets in the treatment of cholestatic disorders. DOI: http://dx.doi.org/10.3329/jbs.v20i0.17647J. bio-sci. 20: 1-23, 2012

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Sommersberger, S., S. Gunawan, T. Elger, T. Fererberger, J. Loibl, M. Huss, A. Kandulski, et al. "P369 Altered fecal bile acid composition in active Ulcerative Colitis." Journal of Crohn's and Colitis 18, Supplement_1 (January 1, 2024): i782. http://dx.doi.org/10.1093/ecco-jcc/jjad212.0499.

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Abstract Background A consistent finding in inflammatory bowel disease (IBD) is an altered composition of fecal bile acids, with an increase in primary bile acids and a decrease in secondary bile acids. It is less clear, whether fecal bile acids could prove to be biomarkers for IBD diagnosis and disease activity. The study aimed to determine correlations between eighteen fecal bile acid species and IBD entity as well as disease severity. Methods Eighteen fecal bile acid species were quantified from stool samples of 62 IBD patients and 17 controls using LC-MS/MS and stable isotope dilution. Bile acid levels were normalized to the dry weight of the fecal homogenates. For calculations, normalized bile acid concentrations and ratios of individual bile acid species to total bile acid levels were used. The p-values were corrected for multiple comparisons. Results In accordance with previous data, we showed that patients with IBD had more primary and less secondary bile acids in their stool compared to healthy controls, with greater differences when comparing healthy controls with ulcerative colitis (UC) than with Crohn´s disease (CD). In CD patients’ fecal calprotectin showed no correlations with any of the bile acids. In UC negative correlations between fecal calprotectin levels and two secondary bile acids, glycine conjugated lithocholic acid (GLCA) and hyodeoxycholic acid (HDCA), and thus total levels of secondary bile acids, existed. Comparing patients with low calprotectin levels (<50 µg/g) and patients with high calprotectin levels (>500 µg/g) in UC revealed that the latter group had lower GLCA and HDCA. Fecal bile acid levels of CD patients did not change with higher calprotectin. Moreover, serum C-reactive protein negatively correlated with the secondary bile acids HDCA, ursodeoxycholic acid, lithocholic acid, taurine conjugated lithocholic acid, deoxycholic acid and its taurine conjugated form in UC but not CD patients. Conclusion To distinguish between IBD subtypes, it may be helpful to note that impaired fecal bile acid homeostasis is specific to patients with active UC.

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Van der Meer, R., and H. T. De Vries. "Differential binding of glycine- and taurine-conjugated bile acids to insoluble calcium phosphate." Biochemical Journal 229, no. 1 (July 1, 1985): 265–68. http://dx.doi.org/10.1042/bj2290265.

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It is demonstrated that bile acids bind to insoluble calcium phosphate at pH values beyond 5.5. Significant binding occurs with glycine-conjugated dihydroxy bile acids. Results indicate that these bile acids are bound in a micellar mode. Taurine conjugation almost completely inhibits the binding of these bile acids to insoluble calcium phosphate. Since glycine-conjugated dihydroxy bile acids are predominant in the rabbit, but not in the rat, our results suggest an explanation for the intriguing species-dependence of casein-induced hypercholesterolaemia, which is high in the rabbit but absent in the rat.

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Weng, Ze-Bin, Yuan-Rong Chen, Jin-Tao Lv, Min-Xin Wang, Zheng-Yuan Chen, Wen Zhou, Xin-Chun Shen, Li-Bin Zhan, and Fang Wang. "A Review of Bile Acid Metabolism and Signaling in Cognitive Dysfunction-Related Diseases." Oxidative Medicine and Cellular Longevity 2022 (March 11, 2022): 1–13. http://dx.doi.org/10.1155/2022/4289383.

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Bile acids are commonly known as one of the vital metabolites derived from cholesterol. The role of bile acids in glycolipid metabolism and their mechanisms in liver and cholestatic diseases have been well studied. In addition, bile acids also serve as ligands of signal molecules such as FXR, TGR5, and S1PR2 to regulate some physiological processes in vivo. Recent studies have found that bile acids signaling may also play a critical role in the central nervous system. Evidence showed that some bile acids have exhibited neuroprotective effects in experimental animal models and clinical trials of many cognitive dysfunction-related diseases. Besides, alterations in bile acid metabolisms well as the expression of different bile acid receptors have been discovered as possible biomarkers for prognosis tools in multiple cognitive dysfunction-related diseases. This review summarizes biosynthesis and regulation of bile acids, receptor classification and characteristics, receptor agonists and signaling transduction, and recent findings in cognitive dysfunction-related diseases.

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Woolbright, Benjamin L., and Hartmut Jaeschke. "Inflammation and Cell Death During Cholestasis: The Evolving Role of Bile Acids." Gene Expression 19, no. 3 (November 4, 2019): 215–28. http://dx.doi.org/10.3727/105221619x15614873062730.

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Cholestasis results in blockage of bile flow whether the point of obstruction occurs extrahepatically or intrahepatically. Bile acids are a primary constituent of bile, and thus one of the primary outcomes is acute retention of bile acids in hepatocytes. Bile acids are normally secreted into the biliary tracts and then released into the small bowel before recirculating back to the liver. Retention of bile acids has long been hypothesized to be a primary cause of the associated liver injury that occurs during acute or chronic cholestasis. Despite this, a surge of papers in the last decade have reported a primary role for inflammation in the pathophysiology of cholestatic liver injury. Furthermore, it has increasingly been recognized that both the constituency of individual bile acids that make up the greater pool, as well as their conjugation status, is intimately involved in their toxicity, and this varies between species. Finally, the role of bile acids in drug-induced cholestatic liver injury remains an area of increasing interest. The purpose of this review is to critically evaluate current proposed mechanisms of cholestatic liver injury, with a focus on the evolving role of bile acids in cell death and inflammation.

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Journal articles on the topic 'Bile Acids'

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