Novel β-catenin/farnesoid X receptor interaction regulates hepatic bile acid metabolism during cholestasis

Hepatology ◽  
2018 ◽  
Vol 67 (3) ◽  
pp. 829-832
Author(s):  
Laurent Ehrlich ◽  
Shannon S. Glaser
Keyword(s):  
Bile Acid ◽  
Acid Metabolism ◽  
Farnesoid X Receptor ◽  
Receptor Interaction ◽  
Bile Acid Metabolism ◽  
Hepatic Bile

Lactoferrin promotes bile acid metabolism and reduces hepatic cholesterol deposition by inhibiting the farnesoid X receptor (FXR)-mediated enterohepatic axis

2019 ◽  
Vol 10 (11) ◽  
pp. 7299-7307 ◽  
Author(s):  
Chen-Jie Ling ◽  
Jia-Ying Xu ◽  
Yun-Hong Li ◽  
Xing Tong ◽  
Huan-Huan Yang ◽  
...  
Keyword(s):  
Body Weight ◽  
Lipid Metabolism ◽  
Bile Acid ◽  
Acid Metabolism ◽  
Farnesoid X Receptor ◽  
Bile Acid Metabolism ◽  
Hepatic Cholesterol ◽  
Reduce Body Weight ◽  
Regulate Lipid Metabolism

Lactoferrin (LF) is a multifunctional glycoprotein that can regulate lipid metabolism, lower cholesterol, reduce body weight, and prevent atherosclerosis.

scholarly journals Farnesoid X Receptor Agonist Treatment Alters Bile Acid Metabolism but Exacerbates Liver Damage in a Piglet Model of Short-Bowel Syndrome

2017 ◽  
Vol 4 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Prue M. Pereira-Fantini ◽  
Susan Lapthorne ◽  
Cormac G.M. Gahan ◽  
Susan A. Joyce ◽  
Jenny Charles ◽  
...  
Keyword(s):  
Bile Acid ◽  
Short Bowel Syndrome ◽  
Liver Damage ◽  
Receptor Agonist ◽  
Acid Metabolism ◽  
Farnesoid X Receptor ◽  
Bile Acid Metabolism ◽  
Short Bowel

scholarly journals Inulin Supplementation Disturbs Hepatic Cholesterol and Bile Acid Metabolism Independent from Housing Temperature

Nutrients ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 3200
Author(s):  
Mira J. Pauly ◽  
Julia K. Rohde ◽  
Clara John ◽  
Ioannis Evangelakos ◽  
Anja Christina Koop ◽  
...  
Keyword(s):  
Bile Acid ◽  
Acid Metabolism ◽  
Plasma Cholesterol ◽  
Cold Treatment ◽  
Short Chain Fatty Acids ◽  
Liver Cholesterol ◽  
Bile Acid Metabolism ◽  
Short Term ◽  
Hepatic Bile ◽  
Brown Adipose

Dietary fibers are fermented by gut bacteria into the major short chain fatty acids (SCFAs) acetate, propionate, and butyrate. Generally, fiber-rich diets are believed to improve metabolic health. However, recent studies suggest that long-term supplementation with fibers causes changes in hepatic bile acid metabolism, hepatocyte damage, and hepatocellular cancer in dysbiotic mice. Alterations in hepatic bile acid metabolism have also been reported after cold-induced activation of brown adipose tissue. Here, we aim to investigate the effects of short-term dietary inulin supplementation on liver cholesterol and bile acid metabolism in control and cold housed specific pathogen free wild type (WT) mice. We found that short-term inulin feeding lowered plasma cholesterol levels and provoked cholestasis and mild liver damage in WT mice. Of note, inulin feeding caused marked perturbations in bile acid metabolism, which were aggravated by cold treatment. Our studies indicate that even relatively short periods of inulin consumption in mice with an intact gut microbiome have detrimental effects on liver metabolism and function.

scholarly journals Effects of Rhein on Bile Acid Homeostasis in Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Zhong Xian ◽  
Jingzhuo Tian ◽  
Lianmei Wang ◽  
Yushi Zhang ◽  
Jiayin Han ◽  
...  
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Acid Metabolism ◽  
Farnesoid X Receptor ◽  
Bile Acid Metabolism ◽  
Edible Plant ◽  
Clinical Dose ◽  
Acid Accumulation ◽  
Liver And Kidney ◽  
Hepatic Transporters

Rhein, the active ingredient of rhubarb, a medicinal and edible plant, is widely used in clinical practice. However, the effects of repeated intake of rhein on liver function and bile acid metabolism are rarely reported. In this work, we investigated the alterations of 14 bile acids and hepatic transporters after rats were administered with rhein for 5 weeks. There was no obvious injury to the liver and kidney, and there were no significant changes in biochemical indicators. However, 1,000 mg/kg rhein increased the liver total bile acid (TBA) levels, especially taurine-conjugated bile acids (t-CBAs), inhibited the expression of farnesoid X receptor (FXR), small heterodimer partner (SHP), and bile salt export pump (BSEP) mRNA, and upregulated the expression of (cholesterol 7α-hydroxylase) CYP7A1 mRNA. Rhein close to the clinical dose (10 mg/kg and 30 mg/kg) reduced the amounts of TBAs, especially unconjugated bile acids (UCBAs), and elevated the expression of FXR and multidrug resistance-associated protein 3 (Mrp3) mRNA. These results denote that rhein is relatively safe to use at a reasonable dose and timing. 30 mg/kg rhein may promote bile acid transport and reduce bile acid accumulation by upregulating the expression of FXR mRNA and Mrp3 mRNA, potentially resulting in the decrease in serum UBCAs.

scholarly journals β-Catenin regulation of farnesoid X receptor signaling and bile acid metabolism during murine cholestasis

Hepatology ◽  
2018 ◽  
Vol 67 (3) ◽  
pp. 955-971 ◽  
Author(s):  
Michael D. Thompson ◽  
Akshata Moghe ◽  
Pamela Cornuet ◽  
Rebecca Marino ◽  
Jianmin Tian ◽  
...  
Keyword(s):  
Bile Acid ◽  
Acid Metabolism ◽  
Farnesoid X Receptor ◽  
Bile Acid Metabolism ◽  
Receptor Signaling

scholarly journals The contribution of bile acid metabolism to the pathogenesis of Clostridioides difficile infection

2021 ◽  
Vol 14 ◽  
pp. 175628482110177
Author(s):  
Benjamin H. Mullish ◽  
Jessica R. Allegretti
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Gut Microbiome ◽  
Acid Metabolism ◽  
Disease Process ◽  
Farnesoid X Receptor ◽  
Bile Acid Metabolism ◽  
Clostridioides Difficile ◽  
Gut Barrier Function ◽  
Clostridioides Difficile Infection

Clostridioides difficile infection (CDI) remains a major global cause of gastrointestinal infection, with significant associated morbidity, mortality and impact upon healthcare system resources. Recent antibiotic use is a key risk factor for the condition, with the marked antibiotic-mediated perturbations in gut microbiome diversity and composition that underpin the pathogenesis of CDI being well-recognised. However, only relatively recently has further insight been gained into the specific mechanistic links between these gut microbiome changes and CDI, with alteration of gut microbial metabolites – in particular, bile acid metabolism – being a particular area of focus. A variety of in vitro, ex vivo, animal model and human studies have now demonstrated that loss of gut microbiome members with bile-metabolising capacity (including bile salt hydrolases, and 7-α-dehydroxylase) – with a resulting alteration of the gut bile acid milieu – contributes significantly to the disease process in CDI. More specifically, this microbiome disruption results in the enrichment of primary conjugated bile acids (including taurocholic acid, which promotes the germination of C. difficile spores) and loss of secondary bile acids (which inhibit the growth of C. difficile, and may bind to and limit activity of toxins produced by C. difficile). These bile acid changes are also associated with reduced activity of the farnesoid X receptor pathway, which may exacerbate C. difficile colitis throughout its impact upon gut barrier function and host immune/inflammatory response. Furthermore, a key mechanism of efficacy of faecal microbiota transplant (FMT) in treating recurrent CDI has been shown to be restoration of gut microbiome bile metabolising functionality; ensuring the presence of this functionality among defined microbial communities (and other ‘next generation’ FMT products) designed to treat CDI may be critical to their success.

scholarly journals Modulation of Bile Acid Metabolism to Improve Plasma Lipid and Lipoprotein Profiles

2021 ◽  
Vol 11 (1) ◽  
pp. 4
Author(s):  
Boyan Zhang ◽  
Folkert Kuipers ◽  
Jan Freark de de Boer ◽  
Jan Albert Kuivenhoven
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Acid Metabolism ◽  
Ldl Cholesterol ◽  
Farnesoid X Receptor ◽  
New Drugs ◽  
Bile Acid Metabolism ◽  
Atherosclerotic Cardiovascular Disease ◽  
Faecal Excretion ◽  
Alcoholic Fatty Liver

New drugs targeting bile acid metabolism are currently being evaluated in clinical studies for their potential to treat cholestatic liver diseases, non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). Changes in bile acid metabolism, however, translate into an alteration of plasma cholesterol and triglyceride concentrations, which may also affect cardiovascular outcomes in such patients. This review attempts to gain insight into this matter and improve our understanding of the interactions between bile acid and lipid metabolism. Bile acid sequestrants (BAS), which bind bile acids in the intestine and promote their faecal excretion, have long been used in the clinic to reduce LDL cholesterol and, thereby, atherosclerotic cardiovascular disease (ASCVD) risk. However, BAS modestly but consistently increase plasma triglycerides, which is considered a causal risk factor for ASCVD. Like BAS, inhibitors of the apical sodium-dependent bile acid transporter (ASBTi’s) reduce intestinal bile acid absorption. ASBTi’s show effects that are quite similar to those obtained with BAS, which is anticipated when considering that accelerated faecal loss of bile acids is compensated by an increased hepatic synthesis of bile acids from cholesterol. Oppositely, treatment with farnesoid X receptor agonists, resulting in inhibition of bile acid synthesis, appears to be associated with increased LDL cholesterol. In conclusion, the increasing efforts to employ drugs that intervene in bile acid metabolism and signalling pathways for the treatment of metabolic diseases such as NAFLD warrants reinforcing interactions between the bile acid and lipid and lipoprotein research fields. This review may be considered as the first step in this process.

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