Bile acids are endogenous molecules that originate from the liver and transport via bile to the intestines. They normally regulate cholesterol homeostasis, stimulate lipid solubilization and mediate metabolic signaling. Early studies implicated that disorders of bile acids compositions and concentrations can cause liver injury. Several hydrophobic bile acids are toxic and ample increases of them in liver may induce cell inflammation, apoptosis and necrosis. While the hydrophilic bile acid, such as ursodeoxycholic acid, has a therapeutic effect on cholestatic liver diseases. Further more, recent researches demonstrate that bile acids have also been implicated in stimulation of liver regeneration. The antagonistic regulation of liver injury and liver regeneration by bile acids may correlate with its composition and concentration. This review will focus on both how different bile acids and different bile acid concentrations play a critical role in liver injury and regeneration.
| Published in | Advances in Biochemistry (Volume 2, Issue 6) |
| DOI | 10.11648/j.ab.20140206.11 |
| Page(s) | 85-89 |
| Creative Commons |
This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited. |
| Copyright |
Copyright © The Author(s), 2014. Published by Science Publishing Group |
Bile Acids, Liver Injury, Liver Regeneration, UDCA
| [1] | Houten, S.M., M. Watanabe, and J. Auwerx, Endocrine functions of bile acids. EMBO J, 2006. 25(7): p. 1419-25. |
| [2] | Li, T. and J.Y. Chiang, Bile Acid signaling in liver metabolism and diseases. J Lipids, 2012. 2012: p. 754067. |
| [3] | Chiang, J.Y., Bile acid metabolism and signaling. Compr Physiol, 2013. 3(3): p. 1191-212. |
| [4] | Allen, K., H. Jaeschke, and B.L. Copple, Bile acids induce inflammatory genes in hepatocytes: a novel mechanism of inflammation during obstructive cholestasis. Am J Pathol, 2011. 178(1): p. 175-86. |
| [5] | Geier, A. and C. Trautwein, Bile acids are "homeotrophic" sensors of the functional hepatic capacity and regulate adaptive growth during liver regeneration. Hepatology, 2007. 45(1): p. 251-3. |
| [6] | Monte, M.J., et al., Changes in the pool of bile acids in hepatocyte nuclei during rat liver regeneration. J Hepatol, 2002. 36(4): p. 534-42. |
| [7] | Bhushan, B., et al., Role of Bile Acids in Liver Injury and Regeneration following Acetaminophen Overdose. Am J Pathol, 2013. 183(5): p. 1518-26. |
| [8] | Fausto, N., J.S. Campbell, and K.J. Riehle, Liver regeneration. Hepatology, 2006. 43(2 Suppl 1): p. S45-53. |
| [9] | Huang, W., et al., Nuclear receptor-dependent bile acid signaling is required for normal liver regeneration. Science, 2006. 312(5771): p. 233-6. |
| [10] | Ishizaki, K., T. Imada, and M. Tsurufuji, Hepatoprotective bile acid 'ursodeoxycholic acid (UDCA)' Property and difference as bile acids. Hepatol Res, 2005. 33(2): p. 174-7. |
| [11] | Baumgartner, U., et al., Different protective effects of tauroursodeoxycholate, ursodeoxycholate, and 23-methyl-ursodeoxycholate against taurolithocholate-induced cholestasis. Dig Dis Sci, 1996. 41(2): p. 250-5. |
| [12] | Fiorucci, S., et al., Protective effects of 6-ethyl chenodeoxycholic acid, a farnesoid X receptor ligand, in estrogen-induced cholestasis. J Pharmacol Exp Ther, 2005. 313(2): p. 604-12. |
| [13] | Russell, D.W., The enzymes, regulation, and genetics of bile acid synthesis. Annu Rev Biochem, 2003. 72: p. 137-74. |
| [14] | Zhang, Y., et al., Effect of bile duct ligation on bile acid composition in mouse serum and liver. Liver Int, 2012. 32(1): p. 58-69. |
| [15] | Rembacz, K., et al., Unconjugated Bile Salts Shuttle through Hepatocyte Peroxisomes for Glycine or Taurine Conjugation. Hepatology, 2008. 48(4): p. 650a-651a. |
| [16] | Hunt, R.D., G.A. Leveille, and H.E. Sauberlich, Dietary Bile Acids and Lipid Metabolism. Iii. Effects of Lithocholic Acid in Mammalian Species. Proc Soc Exp Biol Med, 1964. 115: p. 277-80. |
| [17] | Palmer, R.H., Gallstones Produced Experimentally by Lithocholic Acid in Rats. Science, 1965. 148(3675): p. 1339-40. |
| [18] | Carey, J.B., Jr., et al., The metabolism of bile acids with special reference to liver injury. Medicine (Baltimore), 1966. 45(6): p. 461-70. |
| [19] | Delzenne, N.M., et al., Comparative hepatotoxicity of cholic acid, deoxycholic acid and lithocholic acid in the rat: in vivo and in vitro studies. Toxicol Lett, 1992. 61(2-3): p. 291-304. |
| [20] | Fiorucci, S., et al., Counter-regulatory role of bile acid activated receptors in immunity and inflammation. Curr Mol Med, 2010. 10(6): p. 579-95. |
| [21] | Schoemaker, M.H., et al., Resistance of rat hepatocytes against bile acid-induced apoptosis in cholestatic liver injury is due to nuclear factor-kappa B activation. J Hepatol, 2003. 39(2): p. 153-61. |
| [22] | Costa, A.M., et al., Role of apoptosis in the remodeling of cholestatic liver injury following release of the mechanical stress. Virchows Arch, 2003. 442(4): p. 372-80. |
| [23] | Lee, H.Y., et al., Bile acid regulates MUC2 transcription in colon cancer cells via positive EGFR/PKC/Ras/ERK/CREB, PI3K/Akt/IkappaB/NF-kappaB and p38/MSK1/CREB pathways and negative JNK/c-Jun/AP-1 pathway. Int J Oncol, 2010. 36(4): p. 941-53. |
| [24] | Gujral, J.S., et al., Functional importance of ICAM-1 in the mechanism of neutrophil-induced liver injury in bile duct-ligated mice. Am J Physiol Gastrointest Liver Physiol, 2004. 286(3): p. G499-507. |
| [25] | Lalor, P.F., et al., Vascular adhesion protein-1 mediates adhesion and transmigration of lymphocytes on human hepatic endothelial cells. J Immunol, 2002. 169(2): p. 983-92. |
| [26] | Palmeira, C.M. and A.P. Rolo, Mitochondrially-mediated toxicity of bile acids. Toxicology, 2004. 203(1-3): p. 1-15. |
| [27] | Chipuk, J.E., et al., The BCL-2 family reunion. Mol Cell, 2010. 37(3): p. 299-310. |
| [28] | Ow, Y.P., et al., Cytochrome c: functions beyond respiration. Nat Rev Mol Cell Biol, 2008. 9(7): p. 532-42. |
| [29] | Fang, Y., et al., Bile acids induce mitochondrial ROS, which promote activation of receptor tyrosine kinases and signaling pathways in rat hepatocytes. Hepatology, 2004. 40(4): p. 961-71. |
| [30] | Booth, D.M., et al., Reactive oxygen species induced by bile acid induce apoptosis and protect against necrosis in pancreatic acinar cells. Gastroenterology, 2011. 140(7): p. 2116-25. |
| [31] | Marin, J.J., et al., Mitochondrial genome depletion in human liver cells abolishes bile acid-induced apoptosis: Role of the Akt/mTOR survival pathway and Bcl-2 family proteins. Free Radic Biol Med, 2013. 61C: p. 218-228. |
| [32] | Khan, A.Z. and S.S. Mudan, Liver regeneration: mechanisms, mysteries and more. ANZ J Surg, 2007. 77(1-2): p. 9-14. |
| [33] | Castro, R.E., et al., Identification of microRNAs during rat liver regeneration after partial hepatectomy and modulation by ursodeoxycholic acid. Am J Physiol Gastrointest Liver Physiol, 2010. 299(4): p. G887-97. |
| [34] | Guicciardi, M.E. and G.J. Gores, Ursodeoxycholic acid cytoprotection: dancing with death receptors and survival pathways. Hepatology, 2002. 35(4): p. 971-3. |
| [35] | Gadaleta, R.M., et al., Bile acids and their nuclear receptor FXR: Relevance for hepatobiliary and gastrointestinal disease. Biochim Biophys Acta, 2010. 1801(7): p. 683-92. |
| [36] | Wang, Y.D., et al., Farnesoid X receptor protects liver cells from apoptosis induced by serum deprivation in vitro and fasting in vivo. Mol Endocrinol, 2008. 22(7): p. 1622-32. |
| [37] | Meng, Z., et al., FXR regulates liver repair after CCl4-induced toxic injury. Mol Endocrinol, 2010. 24(5): p. 886-97. |
| [38] | Chen, W.D., et al., Farnesoid X receptor alleviates age-related proliferation defects in regenerating mouse livers by activating forkhead box m1b transcription. Hepatology, 2010. 51(3): p. 953-62. |
| [39] | Pean, N., et al., The receptor TGR5 protects the liver from bile acid overload during liver regeneration in mice. Hepatology, 2013. 58(4): p. 1451-60. |
| [40] | Keitel, V., et al., Expression and function of the bile acid receptor TGR5 in Kupffer cells. Biochem Biophys Res Commun, 2008. 372(1): p. 78-84. |
| [41] | Wang, Y.D., et al., The G-protein-coupled bile acid receptor, Gpbar1 (TGR5), negatively regulates hepatic inflammatory response through antagonizing nuclear factor kappa light-chain enhancer of activated B cells (NF-kappaB) in mice. Hepatology, 2011. 54(4): p. 1421-32. |
| [42] | Watanabe, M., et al., Bile acids induce energy expenditure by promoting intracellular thyroid hormone activation. Nature, 2006. 439(7075): p. 484-9. |
| [43] | Gupta, S., et al., Down-regulation of cholesterol 7alpha-hydroxylase (CYP7A1) gene expression by bile acids in primary rat hepatocytes is mediated by the c-Jun N-terminal kinase pathway. J Biol Chem, 2001. 276(19): p. 15816-22. |
| [44] | Qiao, L., et al., Bile acid regulation of C/EBPbeta, CREB, and c-Jun function, via the extracellular signal-regulated kinase and c-Jun NH2-terminal kinase pathways, modulates the apoptotic response of hepatocytes. Mol Cell Biol, 2003. 23(9): p. 3052-66. |
| [45] | Amaral, J.D., et al., Bile acids: regulation of apoptosis by ursodeoxycholic acid. J Lipid Res, 2009. 50(9): p. 1721-34. |
| [46] | Maton, P.N., G.M. Murphy, and R.H. Dowling, Ursodeoxycholic acid treatment of gallstones. Dose-response study and possible mechanism of action. Lancet, 1977. 2(8052-8053): p. 1297-301. |
| [47] | Soderdahl, G., et al., Ursodeoxycholic acid increased bile flow and affects bile composition in the early postoperative phase following liver transplantation. Transpl Int, 1998. 11 Suppl 1: p. S231-8. |
| [48] | Roma, M.G., et al., Ursodeoxycholic acid in cholestasis: linking action mechanisms to therapeutic applications. Clin Sci (Lond), 2011. 121(12): p. 523-44. |
| [49] | Ros, E., et al., Occult microlithiasis in 'idiopathic' acute pancreatitis: prevention of relapses by cholecystectomy or ursodeoxycholic acid therapy. Gastroenterology, 1991. 101(6): p. 1701-9. |
| [50] | Chun, H.S. and W.C. Low, Ursodeoxycholic acid suppresses mitochondria-dependent programmed cell death induced by sodium nitroprusside in SH-SY5Y cells. Toxicology, 2012. 292(2-3): p. 105-12. |
APA Style
Xiaowen Tang, Lili Ding, Qiaoling Yang, Xiaoyuan Niu, Li Yang, et al. (2014). Advances in Bile Acids-Mediated Liver Injury and Liver Regeneration. Advances in Biochemistry, 2(6), 85-89. https://doi.org/10.11648/j.ab.20140206.11
ACS Style
Xiaowen Tang; Lili Ding; Qiaoling Yang; Xiaoyuan Niu; Li Yang, et al. Advances in Bile Acids-Mediated Liver Injury and Liver Regeneration. Adv. Biochem. 2014, 2(6), 85-89. doi: 10.11648/j.ab.20140206.11
AMA Style
Xiaowen Tang, Lili Ding, Qiaoling Yang, Xiaoyuan Niu, Li Yang, et al. Advances in Bile Acids-Mediated Liver Injury and Liver Regeneration. Adv Biochem. 2014;2(6):85-89. doi: 10.11648/j.ab.20140206.11
Share This Article
Twitter
Linked In
Facebook
Copy
Download@article{10.11648/j.ab.20140206.11,
author = {Xiaowen Tang and Lili Ding and Qiaoling Yang and Xiaoyuan Niu and Li Yang and Zhengtao Wang},
title = {Advances in Bile Acids-Mediated Liver Injury and Liver Regeneration},
journal = {Advances in Biochemistry},
volume = {2},
number = {6},
pages = {85-89},
doi = {10.11648/j.ab.20140206.11},
url = {https://doi.org/10.11648/j.ab.20140206.11},
eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.ab.20140206.11},
abstract = {Bile acids are endogenous molecules that originate from the liver and transport via bile to the intestines. They normally regulate cholesterol homeostasis, stimulate lipid solubilization and mediate metabolic signaling. Early studies implicated that disorders of bile acids compositions and concentrations can cause liver injury. Several hydrophobic bile acids are toxic and ample increases of them in liver may induce cell inflammation, apoptosis and necrosis. While the hydrophilic bile acid, such as ursodeoxycholic acid, has a therapeutic effect on cholestatic liver diseases. Further more, recent researches demonstrate that bile acids have also been implicated in stimulation of liver regeneration. The antagonistic regulation of liver injury and liver regeneration by bile acids may correlate with its composition and concentration. This review will focus on both how different bile acids and different bile acid concentrations play a critical role in liver injury and regeneration.},
year = {2014}
}
TY - JOUR T1 - Advances in Bile Acids-Mediated Liver Injury and Liver Regeneration AU - Xiaowen Tang AU - Lili Ding AU - Qiaoling Yang AU - Xiaoyuan Niu AU - Li Yang AU - Zhengtao Wang Y1 - 2014/11/28 PY - 2014 N1 - https://doi.org/10.11648/j.ab.20140206.11 DO - 10.11648/j.ab.20140206.11 T2 - Advances in Biochemistry JF - Advances in Biochemistry JO - Advances in Biochemistry SP - 85 EP - 89 PB - Science Publishing Group SN - 2329-0862 UR - https://doi.org/10.11648/j.ab.20140206.11 AB - Bile acids are endogenous molecules that originate from the liver and transport via bile to the intestines. They normally regulate cholesterol homeostasis, stimulate lipid solubilization and mediate metabolic signaling. Early studies implicated that disorders of bile acids compositions and concentrations can cause liver injury. Several hydrophobic bile acids are toxic and ample increases of them in liver may induce cell inflammation, apoptosis and necrosis. While the hydrophilic bile acid, such as ursodeoxycholic acid, has a therapeutic effect on cholestatic liver diseases. Further more, recent researches demonstrate that bile acids have also been implicated in stimulation of liver regeneration. The antagonistic regulation of liver injury and liver regeneration by bile acids may correlate with its composition and concentration. This review will focus on both how different bile acids and different bile acid concentrations play a critical role in liver injury and regeneration. VL - 2 IS - 6 ER -
Information
Email: