Download or read book Vitamin D Receptor Regulation of Cholesterol 7 alpha hydroxylase Gene Transcription and Bile Acid Synthesis in Human Hepatocytes written by Shuxin Han and published by . This book was released on 2009 with total page 256 pages. Available in PDF, EPUB and Kindle. Book excerpt: Vitamin D receptor (VDR) plays an important role in the regulation of calcium and phosphate homeostasis and bone formation. Lithocholic acid (LCA) is a potent endogenous ligand of VDR. In cholestasis, LCA levels increase in the liver and intestine. The objective of this study is to test the hypothesis that VDR plays a role in inhibiting the gene expression of cholesterol 7[alpha]-hydroxylase (CYP7A1) and bile acid synthesis in human hepatocytes. Immunoblot analysis has detected VDR proteins in the human hepatoma cell line HepG2 and primary hepatocytes. 1[alpha], 25-dihydroxy-vitamin D3 (1[alpha], 25(OH)2-VD3) or LCA acetate-activated VDR inhibited CYP7A1 mRNA expression and bile acid synthesis, whereas small interfering RNA (siRNA) to VDR completely abrogated VDR inhibition of CYP7A1 in HepG2 cells. LCA or 1[alpha], 25(OH)2-VD3 induced VDR translocation from the cytosol to the nucleus and plasma membrane in human primary hepatocytes. LCA or 1[alpha], 25(OH)2-VD3 activated a tyrosine kinase c-Src and the VDR signaling pathway, which activated c-Raf, an upstream kinase of the MAPK pathway. Kinase inhibition and in vitro kinase assays showed that VDR specifically activated extracellular signal-regulated kinase 1/2 (ERK1/2), which phosphorylated VDR, retinoid X receptor [alpha] (RXR[alpha]) and hepatocyte nuclear factor 4[alpha] (HNF4[alpha]). Mammalian two-hybrid, coimmunoprecipitation, glutathione S-transferase pull-down, and chromatin immunoprecipitation assays show that ligand activated VDR specifically interacts with HNF4[alpha] to block HNF4[alpha] interaction with coactivators. ERK1/2 inhibitors suppressed VDR interaction with HNF4[alpha]. Electrophoretic mobility shift assay and mutagenesis analyses have identified the negative VDR response elements that bind VDR/RXR[alpha] in the human CYP7A1 promoter. Chromatin immunoprecipitation assays show that LCA or 1[alpha], 25(OH)2-VD3 activated ERK1/2 stimulated the recruitment of VDR, RXR[alpha] and co-repressors, but decreased the occupancy of HNF4[alpha] and coactivators to human CYP7A1 chromatin, resulting in the inhibition of CYP7A1 gene transcription. In conclusion, LCA and 1[alpha], 25(OH)2-VD3 caused intracellular translocation of VDR to the plasma membrane and nucleus in human hepatocytes. LCA and VDR activated the c-Raf/MEK/ERK1/2 pathway to regulate VDR inhibition of CYP7A1 in hepatocytes. This study identified a novel bile acid-activated VDR signaling pathway in human hepatocytes. LCA activation of VDR may inhibit bile acid synthesis and protect hepatocytes from cholestatic liver injury.

Download or read book Pregnane X Receptor Regulation of Bile Acid Metabolism and Cholesterol Homeostasis written by Tiangang Li and published by . This book was released on 2006 with total page 189 pages. Available in PDF, EPUB and Kindle. Book excerpt: The nuclear receptor pregnane X receptor (PXR) is activated by bile acids, steroids and drugs and regulates a network of genes in lipid and drug mechanisms. The goal of this study is to investigate the role of PXR in the coordinate regulation of bile acid synthetic and detoxification genes and its implications in cholestatic liver diseases and treatments. Cholesterol 7alpha hydroxylase (CYP7A1) catalyzes the rate-limiting step in the classic bile acids synthetic pathway and plays a key role in controlling bile acids homeostasis. Quantitative real-time PCR (Q-PCR) showed human PXR agonist rifampicin inhibited CYP7A1 mRNA expression in primary human hepatocytes. Mammalian two-hybrid assays, co-immunoprecipitation (co-IP) assays and chromatin immunoprecipitation (ChIP) assay revealed that ligand-activated PXR strongly interacted with HNF4alpha, the key activator of human CYP7A1, and blocked HNF4alpha interaction with co-activator PGC-1alpha, thus resulted in inhibition of CYP7A1. CYP3A4 is the most abundant cytochrome P450 monooxygenase expressed in human liver and intestine. Bile acids and drugs-activated PXR induces CYP3A4, which converts toxic bile acids to non-toxic metabolites for excretion. Studies using Q-PCR, reporter assays, GST pull-down assays and ChIP assays revealed that PXR strongly induced CYP3A4 gene transcription by interacting with HNF4alpha, SRC-1 and PGC-1alpha. SHP, a negative nuclear receptor, reduced PXR recruitment of HNF4alpha and SRC-1 to the CYP3A4 chromatin and inhibited CYP3A4. Interestingly, PXR concomitantly inhibited SHP gene transcription and maximized the PXR induction of CYP3A4. Taken together, PXR inhibits CYP7A1 to reduce bile acid synthesis and induces CYP3A4 to detoxify bile acid. Thus, PXR may play a protective role against cholestasis. Drugs targeted to PXR may be developed for treating cholestatic liver diseases induced by bile acids and drugs. Mitochondrial sterol 27-hydroxylase (CYP27A1) catalyzes the side-chain cleavage reaction in bile acid synthetic pathways and 27-hydroxylation of cholesterol mainly in the peripheral tissues. Q-PCR revealed that rifampicin induced CYP27A1 mRNA expression in the intestine-derived Caco2 cells, but not in primary human hepatocytes and HepG2 cells. Rifampicin stimulated CYP27A1 gene transcription in cholesterol laden Caco2 cells and increased intracellular 27HOC, which stimulates cholesterol efflux by induction of cholesterol efflux transporters ABCA1 and ABCG1. Mutagenesis analysis, electrophoretic mobility shift assay and ChIP assays identified a functional PXR binding site in the human CYP27A1 gene. These data suggest that 27-hydroxycholesterol is an endogenous LXRalpha ligand and the PXR/CYP27A1/LXRalpha signaling pathway regulate cholesterol efflux in intestine cells. Results revealed an intestine-specific regulation of human CYP27A1 gene by PXR and suggested a novel role for PXR in cholesterol metabolism and detoxification in the intestine.

Download or read book Cytokine Repression of the Human Sterol 12 alpha hydroxylase cyp8b1 Gene an Alternative Mechanism for Bile Acid Suppression of CYP8B1 written by Asmeen Bhatt and published by . This book was released on 2006 with total page 228 pages. Available in PDF, EPUB and Kindle. Book excerpt: Bile acids, synthesized from precursor cholesterol molecules, serve as an important mechanism for elimination of excess cholesterol from the body. Bile acid synthesis is tightly regulated since excess bile acids are toxic and can cause liver damage. Bile acids inhibit their own synthesis by inhibiting the bile acid biosynthetic genes. Cholesterol 7[alpha] -hydroxylase (CYP7A1) is the rate-limiting enzyme of classic bile acid biosynthesis, which synthesizes two primary bile acids, cholic acid (CA) and chenodeoxycholic acid (CDCA) in the liver. Sterol 12[alpha] -hydroxylase (CYP8B1) catalyzes CA synthesis in the liver and is feedback inhibited by bile acids. In addition to activating farnesoid X receptor (FXR, nuclear receptor subfamily 1H4, NR1H4), bile acids also induce the release of inflammatory cytokines, like interleukin 1[beta] (IL-1[beta]) from Kupffer cells in the liver. The objective of this study was to investigate the mechanism by which inflammatory cytokines inhibit human CYP8B1 gene transcription. Real time PCR assays revealed that both CDCA and IL-1[beta] ; markedly reduced CYP8B1, CYP7A1, and nuclear receptor hepatocyte nuclear factor 4[alpha] (HNF4[alpha], NR2A1) mRNA expression levels in human primary hepatocytes. However, CDCA induced, but IL-1[beta] reduced the negative nuclear receptor, small heterodimer partner (SHP, NR0B2) mRNA expression. IL-1[beta] inhibited human CYP8B1 reporter activity only in liver cells, and a c-Jun N-terminus kinase(JNK)-specific inhibitor blocked IL-1[beta] inhibition. Activated JNK1 or c-Jun inhibited, whereas their dominant negative forms blocked IL-1[beta] inhibition of CYP8B1 transcription. Mutagenesis analyses mapped an IL-1[beta] response element to a previously identified bile acid response element, which contains an HNF4[alpha] binding site. Furthermore, IL-1beta] inhibited HNF4[alpha] gene transcription, protein expression and binding to the CYP8B1 gene. JNK1 phosphorylated HNF4[alpha] and a JNK-specific inhibitor blocked the IL-1[beta]; inhibition of HNF4[alpha] expression. Expression of c-Jun, a downstream target of the JNK pathway, was induced by both IL-1[beta] and CDCA in primary human hepatocytes. c-Jun inhibited the HNF4[alpha] and coactivator peroxisome proliferator-activated receptor [gamma] co-activator-1[alpha] (PGC-1[alpha]) mediated trans-activation of CYP8B1 reporter activity. Coimmunoprecipitation revealed an interaction between c-Jun and HNF4[alpha], which was confirmed by GST pull down assay. IL-1[beta] increased the ratio of c-Jun or phosphorylated c-Jun bound to HNF4[alpha] in HepG2 cells. Chromatin immunoprecipitation (ChIP) assay revealed that c-Jun did not affect HNF4[alpha] binding but blocked HNF4[alpha] recruitment of PGC-1[alpha] to the CYP8B1 chromatin. This study also showed that HNF4[alpha] stimulated the gene expression of SHP by binding to the promoter of the latter. The results suggest that IL-1[beta] inhibits CYP8B1 gene transcription, in a SHP-independent manner via the JNK pathway that inhibits HNF4[alpha] gene expression and its DNA-binding ability. IL-1[beta] also induces c-Jun, which blocks HNF4[alpha] recruitment of PGC-1[alpha] to CYP8B1 chromatin. This mechanism may play an important role in the adaptive response to inflammatory cytokines and in the protection of the liver during cholestasis.

Download or read book Cholesterol 7 Alpha hydroxylase is Regulated Post translationally by AMPK written by Mauris E. C. Nnamani and published by . This book was released on 2009 with total page 205 pages. Available in PDF, EPUB and Kindle. Book excerpt: Type II diabetes and dyslipidemia are common metabolic disorders resulting in a higher risk of cardiovascular disease, larger bile acid pools, and excretion rates; suggesting an association between abnormal bile acid and cholesterol biosynthesis with type II diabetes and cardiovascular disease. The rate at which cholesterol is converted to bile acids is determined by the activity of the liver enzyme, cholesterol 7 alpha-hydroxylase. AMP-activated protein kinase (AMP), has long been recognized as regulating cholesterol synthesis by controlling 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, the second and rate-limiting step of cholesterol synthesis. In addition, AMPK is significant for its roles in energy metabolism. 5-aminoimidazole-4-carboxamide-1-beta-D-ribofuranoside (AICAR) is an activator of AMPK. Previous work in the Stroup lab have shown that AICAR treatment changes the rate at which the human hepatoma cell line (HepG2) synthesizes bile acids without significantly changing message RNA levels, as measured with real-time PCR. Also recombinant human cholesterol 7-alpha-hydroxylase can be covalently modified by commercially available AMPK in kinase assays. To test the hypothesis that cholesterol 7 alpha-hydroxylase activity can be regulated posttranslationally by phosphorylation, catalytically active cholesterol 7 alpha-hydroxylase was expressed in E. coli, purified and reacted with purified AMPK, cAMP-dependant protein kinase (PKA), and protein kinase C (PKC). Cholesterol 7 alpha-hydroxylase activity was determined by measuring the conversion of cholesterol into 7 alpha-hydroxycholesterol by recombinant CYP7A1 using LC-MS. The product was measured without chemical derivation with an orthogonal atmospheric pressure chemical ionization source (APCI) detector, using a method developed for this study. The effects of the kinases on activity of the recombinant enzyme were compared to that of extracts prepared from HepG2 cells. The activities measured from the kinase-treated extracts were significantly different than controls, and were specific to the kinases used. Site-directed mutagenesis was performed to determine phosphorylation sites responsible for the effects noticed by kinase activity. AMPK repressed E. coli-expressed recombinant CYP7A1 enzymatic activity by phosphorylating S252. The finding that the activity of cholesterol 7 alpha-hydroxylase can be regulated post-translationally by AMPK provides a possible mechanism of coordinating cholesterol disposal with cholesterol synthesis.

Download or read book Vitamin D Receptor VDR and Cholesterol Homeostasis written by Holly Quach and published by . This book was released on 2016 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Vitamin D deficiency is speculated to play a role in hypercholesterolemia. However, there has been little molecular evidence to link the two until recent evidence identified the vitamin D receptor (VDR) and its natural ligand, 1Îą,25-dihydroxyvitamin D3 [1,25(OH)2D3], as key regulators of cholesterol metabolism. In the liver, 1,25(OH)2D3-liganded VDR directly inhibited the small heterodimer partner (Shp) to increase expression of cholesterol 7Îą-hydroxylase (Cyp7a1), the rate-limiting enzyme for cholesterol metabolism to bile acids, a mechanism independent of the farnesoid X receptor. Vitamin D deficiency was established in mice after 8 weeks of the D-deficient diet, which resulted in decreased levels of plasma and liver 1,25(OH)2D3, downregulation of hepatic Vdr and Cyp7a1, and elevation of Shp. Consequently, higher plasma and liver cholesterol levels were observed. Intervention with 1,25(OH)2D3 or vitamin D3 reversed the altered expression of these cholesterol-regulating genes and lowered cholesterol levels back to baseline levels. The correlations between liver cholesterol vs. liver 1,25(OH)2D3 and Cyp7a1 expression in mice were also found in human liver tissue, suggesting that the VDR could be a potential therapeutic target for cholesterol lowering. However, the therapeutic utility of 1,25(OH)2D3 is limited by hypercalcemia and by its feedback control mechanisms. When given exogenously, 1,25(OH)2D3 triggered inhibition of its synthesis enzyme (Cyp27b1) but induction of its degradation enzyme (Cyp24a1) in a dose-dependent manner, events that are predicted by compartmental and physiologically-based pharmacokinetic/pharmacodynamic modeling. These models provide a foundation for predicting 1,25(OH)2D3 disposition for inter-species scaling and for exploration of alternative dosing schemes and routes of administration to describe the dynamics of 1,25(OH)2D3 in its new therapeutic roles. Overall, these findings highlight the importance of vitamin D status and the VDR as regulators of hypercholesterolemia.

Download or read book In Vitro Characterization of the Cholesterol 7 alpha hydroxylase Gene written by Roya Bashirzadeh and published by . This book was released on 1992 with total page 102 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Biological Roles of the Vitamin D Receptor in the Regulation of Transporters and Enzymes on Drug Disposition Including Cytochrome P450 CYP7A1 on Cholesterol Metabolism written by Edwin C. Y. Chow and published by . This book was released on 2012 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: Nuclear receptors play significant roles in the regulation of transporters and enzymes to balance the level of endogenous molecules and to protect the body from foreign molecules. The vitamin D receptor (VDR) and its natural ligand, 1alpha,25-dihydroxyvitamin D3 [1,25(OH)2D3], was shown to upregulate rat ileal apical sodium dependent bile acid transporter (Asbt) to increase the reclamation of bile acids, ligands of the farnesoid X receptor (FXR). FXR is considered to be an important, negative regulator of the cholesterol metabolizing enzyme, Cyp7a1, which metabolizes cholesterol to bile acids in the liver. In rats, decreased Cyp7a1 and increased P-glycoprotein/multidrug resistance protein 1 (P-gp/Mdr1) expressions pursuant to 1,25(OH)2D3 treatment was viewed as FXR effects in which hepatic VDR protein is poorly expressed. In contrast, changes in rat intestinal and renal transporters such as multidrug resistance associated proteins (Mrp2, Mrp3, and Mrp4), Asbt, and P-gp after administration of 1,25(OH)2D3 were attributed directly as VDR effects due to higher VDR levels expressed in these tissues. Higher VDR expressions were found among mouse hepatocytes compared to those in rats. Hence, fxr(-/-) and fxr(+/+) mouse models were used to discriminate between VDR vs. FXR effects in murine livers. Hepatic Cyp7a1 in mice was found to be upregulated with 1,25(OH)2D3 treatment, via the derepression of the short heterodimer partner (SHP). Putative VDREs, identified in mouse and human SHP promoters, were responsible for the inhibitory effect on SHP. The increase in hepatic Cyp7a1 expression and decreased plasma and liver cholesterol were observed in mice prefed with a Western diet. A strong correlation was found between tissue Cyp7a1 and P-gp changes and 1,25(OH)2D3 plasma and tissue concentrations, confirming that VDR plays an important role in the disposition of xenobiotics and cholesterol metabolism. Moreover, renal and brain Mdr1a/P-gp were found to be directly upregulated by the VDR in mice, and concomitantly, increased renal and brain secretion of digoxin, a P-gp substrate, in vivo. The important observations: the cholesterol lowering and increased brain P-gp efflux activity properties suggest that VDR is a therapeutic target for treatment of hypercholesterolemia and Alzheimer's diseases, since beta amyloid, precursors of plague, are P-gp substrates.

Download or read book Molecular Pathology of Liver Diseases written by Satdarshan P. S. Monga and published by Springer Science & Business Media. This book was released on 2010-12-14 with total page 920 pages. Available in PDF, EPUB and Kindle. Book excerpt: Cellular and Molecular Pathology of the Liver is extensive, complex and ranges from the understanding the basic molecular mechanisms that dictate everything from liver homeostasis to liver disease. Molecular Pathology of the liver is complicated due to some of the important functions inherent and unique to the Liver, including its innate ability to regenerate and the multitude of functions it plays for the wellbeing of an organism. With all this in mind, Molecular Pathology of Liver Diseases is organized in different sections, which will coherently and cohesively present the molecular basis of hepatic physiology and pathology. The first two sections are key to understanding the liver anatomy and physiology at a cellular level and go on to define the molecular mechanics in various liver cell types. These sections also cover the existing paradigms in liver development, regeneration and growth. The next section is key to understanding the Molecular Pathology unique to liver diseases and associated phenotypes. The final sections are geared towards the existing knowledge of the molecular basis of many common and uncommon liver diseases in both neoplastic and non-neoplastic areas including pathologies associated with intra-hepatic and extra-hepatic biliary tree. Thus, this textbook is a one-stop reference for comprehending the molecular mechanisms of hepatic pathobiology. It is clearly unique in its format, readability and information and thus will be an asset to many in the field of Pathology and other disciplines.

Download or read book Bile Acids and Their Receptors written by Stefano Fiorucci and published by Springer Nature. This book was released on 2019-09-03 with total page 378 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book focusses on the latest results related to the field of bile acids as signaling molecules and describes how these receptors have become a major pharmacological target. It covers all major areas of research in this field, from genetics, chemistry, in silico modeling, molecular biology to clinical applications, offering a cross-country view of the functional role of bile acids as signaling molecules, virtually acting on all major areas of metabolism. While FXR and GPBAR1 are essential bile acid sensors that integrate the de novo bile acid synthesis with intestinal microbiota and liver metabolism, in a broader sense, BARs play a pathogenic role in the development of common human alignments including liver, intestinal and metabolic disorders, such as steatosis (NAFLD) and steato-hepatitis (NASH), diabetes, obesity and atherosclerosis.

Download or read book Liver Disease in Children written by Frederick J. Suchy and published by Cambridge University Press. This book was released on 2021-03-18 with total page 875 pages. Available in PDF, EPUB and Kindle. Book excerpt: Liver disease in children is increasing in prevalence, placing a huge burden on healthcare systems and often requiring long-term management. Offering an integrative approach to the science and clinical practice of pediatric hepatology, this is the definitive reference text for improved diagnosis and treatment strategies. In the new edition of this authoritative text, chapters have been thoroughly revised in line with major advances in the field, such as recognizing the increased frequency of fatty liver disease, and how genetic testing has the potential to establish earlier diagnoses for a variety of diseases. Disorders covered include cholestasis, metabolic disorders and hepatitis, with their presentation across the spectrum of infancy, childhood and adolescence discussed. The indications and surgical aspects of liver transplant are explained and post-transplant care is described in detail. This is a valuable resource for pediatricians, hepatologists, gastroenterologists and all clinicians involved in the care of children with liver diseases.

Download or read book Atherosclerosis and Oxidant Stress A New Perspective written by Jordan L Holtzman and published by Springer Science & Business Media. This book was released on 2007-09-26 with total page 255 pages. Available in PDF, EPUB and Kindle. Book excerpt: Vascular injury is initiated by oxidant injury to the vessel wall. This volume is organized around the role of oxidant damage in this disease process and provides a collection of the most recent studies, representing various disciplines that can serve as the basis for further improvements in our understanding and control of cardiovascular and cerebral vascular disease.

Download or read book The Liver written by Irwin M. Arias and published by John Wiley & Sons. This book was released on 2020-03-09 with total page 1156 pages. Available in PDF, EPUB and Kindle. Book excerpt: Bridging the gap between basic scientific advances and the understanding of liver disease — the extensively revised new edition of the premier text in the field. The latest edition of The Liver: Biology and Pathobiology remains a definitive volume in the field of hepatology, relating advances in biomedical sciences and engineering to understanding of liver structure, function, and disease pathology and treatment. Contributions from leading researchers examine the cell biology of the liver, the pathobiology of liver disease, the liver’s growth, regeneration, metabolic functions, and more. Now in its sixth edition, this classic text has been exhaustively revised to reflect new discoveries in biology and their influence on diagnosing, managing, and preventing liver disease. Seventy new chapters — including substantial original sections on liver cancer and groundbreaking advances that will have significant impact on hepatology — provide comprehensive, fully up-to-date coverage of both the current state and future direction of hepatology. Topics include liver RNA structure and function, gene editing, single-cell and single-molecule genomic analyses, the molecular biology of hepatitis, drug interactions and engineered drug design, and liver disease mechanisms and therapies. Edited by globally-recognized experts in the field, this authoritative volume: Relates molecular physiology to understanding disease pathology and treatment Links the science and pathology of the liver to practical clinical applications Features 16 new “Horizons” chapters that explore new and emerging science and technology Includes plentiful full-color illustrations and figures The Liver: Biology and Pathobiology, Sixth Edition is an indispensable resource for practicing and trainee hepatologists, gastroenterologists, hepatobiliary and liver transplant surgeons, and researchers and scientists in areas including hepatology, cell and molecular biology, virology, and drug metabolism.

Download or read book The Biology of Cholesterol and Related Steroids written by N. B. Myant and published by Butterworth-Heinemann. This book was released on 2014-04-24 with total page 925 pages. Available in PDF, EPUB and Kindle. Book excerpt: The Biology of Cholesterol and Related Steroids focuses on the study of sterols in relation to living organisms. The publication first takes a look at the analysis of sterols and related steroids and the distribution of sterols and related steroids in nature, as well as the processes of extraction and separation and presence of sterols in plants, fungi, vertebrates, and invertebrates. The text then ponders on biosynthesis of sterols and metabolism of cholesterol. Topics include formation of fatty acid esters of cholesterol, steroid hormones, biosynthetic pathway to sterols, reaction mechanisms, and comparative aspects of sterol synthesis. The manuscript examines the developmental aspects of cholesterol metabolism and sterols in biological membranes. The book also reviews cholesterol synthesis in animal tissues, sterol metabolism in isolated cells, and epidemiology of the plasma cholesterol. Discussions focus on selection of statistical populations, genetic influences, regulation of sterol synthesis, general aspects of sterol metabolism, and removal of cell cholesterol in vivo. The publication is a dependable source of data for biochemists and readers interested in the biology of cholesterol and steroids.

Download or read book Bile Acids and Cholestasis written by G. Paumgartner and published by Springer. This book was released on 1999-06-30 with total page 318 pages. Available in PDF, EPUB and Kindle. Book excerpt: Since the last International Bile Acid Meeting in Freiburg in 1996, considerable progress has been made in several areas of bile acid research. The different pathways of bile acid synthesis and their regulation have been further characterized. The molecular mechanisms for biliary secretion of bile acids have been elucidated and genetic defects of bile acid transport have been defined. Injurious as well as protective effects of different bile acids on the liver have been further studied. Finally, the beneficial effects of ursodeoxycholic acid in cholestatic liver diseases have been substantiated and the potential mechanisms of action have been explored. This book, the proceedings of the Falk Symposium No. 108 (XV International Bile Acid Meeting), held in Titisee, Germany, October 12-13, 1998, is dedicated to both basic and clinical aspects of bile acid research with a focus on bile acids and cholestasis.

Download or read book Sterols and Bile Acids written by and published by Elsevier. This book was released on 1985-01-01 with total page 465 pages. Available in PDF, EPUB and Kindle. Book excerpt: Sterols and Bile Acids

Download or read book Cholestatic Liver Disease written by Elizabeth J. Carey and published by Springer. This book was released on 2014-07-18 with total page 265 pages. Available in PDF, EPUB and Kindle. Book excerpt: Since the publication of the first edition, there have been advances in both the diagnosis and the management of many of the cholestatic liver diseases. Cholestatic Liver Disease, Second Edition thoroughly updates the topics previously addressed, such as primary biliary cirrhosis, primary sclerosing cholangitis and cholestatic variants of drug hepatotoxicity and viral disease. New treatments, such as the development of the farnesoid X receptor agonists for the treatment of PBC, are highlighted. Current guidelines and areas of uncertainty are also covered. Additionally, new chapters have been added to reflect the changing landscape of cholestatic liver disease. Cholestatic Liver Disease, Second Edition is a concise yet comprehensive summary of the current status of the field and is of value to clinicians and researchers interested in patients with cholestatic liver disease provide that will help to guide patient management and stimulate investigative efforts.

Download or read book Bile Salt Metabolism written by Leon Schiff and published by . This book was released on 1969 with total page 328 pages. Available in PDF, EPUB and Kindle. Book excerpt: