Metabolism of bile acids, liver diseases and microbiome
https://doi.org/10.22416/1382-4376-2018-28-2-4-10
Abstract
Aim of review. To present the modern data on interrelation of bile acid (BA) metabolism, microbiome and liver diseases. Summary. Bile acids are important signaling molecules that regulate lipid and glucose metabolism. Enterohepatic circulation of BA plays the central role in nutrient absorption and metabolic regulation. Data of investigations demonstrate interrelation of BA, intestinal microbiome and liver diseases. In particular, the role of BA metabolism disorders in development of non-alcoholic fatty liver disease is extensively studied. Sequestrants of BA are under study as putative BA and glucose metabolism regulators then draws interest from practical point of view. Conclusion. Bile acids carry out multiple physiological functions. The link between BA metabolism, liver disease and intestinal microbiome is demonstrated by numerous investigations.
About the Authors
Yu. V. Yevsyutina
National Research Center for Preventive Medicine
Russian Federation
Russian Federation
V. T. Ivashkin
Sechenov First Moscow State Medical University (Sechenov University)
Russian Federation
Russian Federation
References
1. Chiang Y.L. Bile Acid Metabolism and Signaling. Compr Physiol 2013; 3(3):1191-212.
2. Boyer J.L. Bile Formation and Secretion. Compr Physiol 2013; 3(3):1035-78.
3. Li T., Apte U. Bile acid metabolism and signaling in cholestasis, inflammation and cancer. Adv Pharmacol 2015; 74:263-302.
4. Dawson Р.A., Karpen S.J. Intestinal transport and metabolism of bile acids. J Lipid Res 2015; 56(6):1085-99.
5. Ridlon J.M., Harris S.C., Bhowmik S. et al. Consequences of bile salt biotransformations by intestinal bacteria. Gut Microbes 2016; 7(1):22-39.
6. Li T., Chiang Y.L. Bile acids as metabolic regulators. Curr Opin Gastroenterol 2015; 31(2):159-65.
7. Dawson P.A., Hubbert M.L., Rao A. Getting the mOST from OST: Role of organic solute transporter, OSTalphaOSTbeta, in bile acid and steroid metabolism. Biochim Biophys Acta 2010; 1801:994-1004.
8. Vallim de Aguiar T.Q., Tarling E.J., Edwards P.A. Pleiotropic Roles of Bile Acids in Metabolism. Cell Metab 2013; 17(5):657-69.
9. Bajaj J.S., Ridlon J.M., Hylemon P.B. et al. Linkage of gut microbiome with cognition in hepatic encephalopathy. Am J Physiol Gastrointest Liver Physiol 2012; 302:16875.
10. Bajaj J.S., Hylemon P.B., Ridlon J.M. et al. Colonic mucosal microbiome differs from stool microbiome in cirrhosis and hepatic encephalopathy and is linked to cognition and inflammation. Am J Physiol Gastrointest Liver Physiol 2012; 303:675-85.
11. Kakiyama G., Pandak W.M., Gillevet P.M. et al. Modulation of the fecal bile acid profile by gut microbiota in cirrhosis. J Hepatol 2013; 58(5):949-55.
12. Ridlon J.M., Kang D.J., Hylemon P.B. et al. Bile Acids and the Gut Microbiome. Curr Opin Gastroenterol 2014; 30(3):332-8.
13. Bajaj J.S., Heuman D.M., Hylemon P.B. et al. The Cirrhosis Dysbiosis Ratio defines Changes in the Gut Microbiome Associated with Cirrhosis and its Complications. J Hepatol 2014; 60(5):940-7.
14. Islam K.B., Fukiya S., Hagio M. et al. Bile acid is a host factor that regulates the composition of the cecal microbiota in rats. Gastroenterology 2011;141(5):1773-81.
15. Tilg H., Moschen А.R., Roden М. NAFLD and diabetes mellitus. Nat Rev Gastroenterol Hepatol 2017; 14:32-42.
16. Zhu Y., Liu H., Zhang M. et al. Fatty liver diseases, bile acids, and FXR. Acta Pharm Sin B 2016; 6(5):409-12.
17. Xu J.Y., Li Z.P., Zhang L. et al. Recent insights into farnesoid X receptor in non-alcoholic fatty liver disease. World J Gastroenterol 2014:7; 20(37):13493-500.
18. Mudaliar S., Henry R., Sanyal A.J. et al. Efficacy and Safety of the Farnesoid X Receptor Agonist Obeticholic Acid in Patients With Type 2 Diabetes and Nonalcoholic Fatty Liver Disease. Gastroenterology 2013; 145:574-82.
19. Neuschwander-Tetri B.A., Loomba R., Sanyal A.J. et al. Farnesoid X nuclear receptor ligand obeticholic acid for non-cirrhotic, non-alcoholic steatohepatitis (FLINT): a multicentre, randomised, placebo-controlled trial. Lancet 2015; 385:956-65.
20. Kuribayashi H., Miyata M., Yamakawa H. et al. Enterobacteria-mediated deconjugation of taurocholic acid enhances ileal farnesoid X receptor signaling. Eur J Pharmacol 2012; 697(1-3):132-8.
21. Sayin S.I., Wahlstrom A., Felin J. et al. Gut microbiota regulates bile acid metabolism by reducing the levels of tauro-beta-muricholic acid, a naturally occurring FXR antagonist. Cell Metab 2013; 17(2):225-35.
22. Swann J.R., Want E.J., Geier F.M. et al. Systemic gut microbial modulation of bile acid metabolism in host tissue compartments. Proc Nat Acad Sci USA 2011; 108(Suppl 1):4523-30.
23. Ryan K.K., Tremaroli V., Clemmensen C. et al. FXR is a molecular target for the effects of vertical sleeve gastrectomy. Nature 2014; 509(7499):183-8.
24. Bashiardes S., Shapiro H., Rozin S. et al. Non-alcoholic fatty liver and the gut microbiota. Mol Metab 2016; 5(9):782-94.
25. Mouzaki M., Wang A.Y., Bandsma R. et al. Bile acids and dysbiosis in non-alcoholic fatty liver disease. PloS One 2016; 11(5): e0151829.
26. Levy M., Thaiss C.A., Zeevi D. et al. Microbiotamodulated metabolites shape the intestinal microenvironment by regulating NLRP6 inflammasome signaling. Cell 2015 Dec 3;163(6):1428-43.
27. Goldberg R.B., Fonseca V.A., Truitt K.E. et al. Efficacy and safety of colesevelam in patients with type 2 diabetes mellitus and inadequate glycemic control receiving insulinbased therapy. Arch Intern Med 2008; 168:1531-40.
28. Sonne D.P., Hansen M., Knop F.K. Bile acid sequestrants in type 2 diabetes: potential effects on GLP1 secretion. European journal of endocrinology. Eur Federat Endocr Soc 2014; 171:47-65.
29. Holst J.J. The physiology of glucagon-like peptide 1. Physiol Rev 2007; 87:1409-39.
30. Thomas C., Gioiello A., Noriega L. et al. TGR5-mediated bile acid sensing controls glucose homeostasis. Cell Metab 2009; 10:167-77.
31. Harach T., Pols T.W., Nomura M. et al. TGR5 potentiates GLP-1 secretion in response to anionic exchange resins. Sci Report 2012; 2:430.
32. Potthoff M.J., Potts A., He T. et al. Colesevelam suppresses hepatic glycogenolysis by TGR5-mediated induction of GLP-1 action in DIO mice. Am J Physiol Gastrointest Liv Physiol 2013; 304:371-80.
33. Hofmann A.F. Bile acid sequestrants improve glycemic control in type 2 diabetes: a proposed mechanism implicating glucagon-like peptide 1 release. Hepatology 2011; 53:1784.
34. Devkota S., Wang Y., Musch M.W. et al. Dietary fatinduced taurocholic acid promotes pathobiont expansion and colitis in Il10-/mice. Nature 2012; 487:104-8.
35. Devkota S., Chang E.B. Interactions between diet, bile acid metabolism, gut microbiota, and inflammatory bowel diseases. Dig Dis 2015; 33:351-6.
36. Caesar R., Tremaroli V., Kovatcheva-Datchary P. et al. Crosstalk between Gut Microbiota and Dietary Lipids Aggravates WAT Inflammation through TLR Signaling. Cell Metab 2015; 22:658-68.
37. Lessa F.C., Mu Y., Bamberg W.M. et al. Burden of Clostridium difficile infection in the United States. N Engl J Med 2015; 26; 372(9):825-34.
38. van Nood E., Vrieze A., Nieuwdorp M. et al. Duodenal infusion of feces for recurrent Clostridium difficile. N Engl J Med 2013; 368(22):407-15.
39. Buffie C.G., Bucci V., Stein R.R. et al. Precision microbiome reconstitution restores bile acid mediated resistance to Clostridium difficile. Nature 2015; 517(7533):205-8.
40. Wilson K.H., Kennedy M.J., Fekety F.R. Use of sodium taurocholate to enhance spore recovery on a medium selective for Clostridium difficile. J Clin Microbiol 1982; (3):443-6.
41. Sorg J.A., Sonenshein A.L. Inhibiting the initiation of Clostridium difficile spore germination using analogs of chenodeoxycholic acid, a bile acid. J Bacteriol 2010; 192(19):4983-90.
42. Sorg J.A., Sonenshein A.L. Bile salts and glycine as cogerminants for Clostridium difficile spores. J Bacteriol 2008; 190(7):2505-12.
43. Francis M.B., Allen C.A., Sorg J.A. Muricholic acids inhibit Clostridium difficile spore germination and growth. PLoS One 2013; 8(9):e73653.
44. Francis M.B., Allen C.A., Shrestha R. et al. Bile acid recognition by the Clostridium difficile germinant receptor, CspC, is important for establishing infection. PLoS Pathog 2013; 9(5):e1003356.
Review
For citations:
Yevsyutina Yu.V., Ivashkin V.T. Metabolism of bile acids, liver diseases and microbiome. Russian Journal of Gastroenterology, Hepatology, Coloproctology. 2018;28(2):4-10. (In Russ.) https://doi.org/10.22416/1382-4376-2018-28-2-4-10
Views:
2666
Email this article 
