Polysaccharides from fermented Asparagus officinalis with Lactobacillus plantarum NCU116 alleviated liver injury via modulation of glutathione homeostasis, bile acid metabolism, and SCFA production

2020 ◽  
Vol 11 (9) ◽  
pp. 7681-7695
Author(s):  
Zhihong Zhang ◽  
Songtao Fan ◽  
Danfei Huang ◽  
Tao Xiong ◽  
Shaoping Nie ◽  
...  
Keyword(s):  
Bile Acid ◽  
Liver Injury ◽  
Lactobacillus Plantarum ◽  
Acid Metabolism ◽  
Asparagus Officinalis ◽  
Expression Level ◽  
Superior Performance ◽  
Bile Acid Metabolism ◽  
Bile Acid Receptors ◽  
Glutathione Homeostasis

FAOP showed superior performance by promoting GSH biosynthesis, normalizing the expression level of bile acid receptors and related enzymes, and upregulating hepatic SCFA receptors and fecal SCFA production.

scholarly journals Beneficial bile acid metabolism from Lactobacillus plantarum of food origin

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Roberta Prete ◽  
Sarah Louise Long ◽  
Alvaro Lopez Gallardo ◽  
Cormac G. Gahan ◽  
Aldo Corsetti ◽  
...  
Keyword(s):  
Bile Acid ◽  
Lactobacillus Plantarum ◽  
Acid Metabolism ◽  
Bile Acid Metabolism

scholarly journals Fibroblast Growth Factor 21 Response in a Preclinical Alcohol Model of Acute-on-Chronic Liver Injury

2021 ◽  
Vol 22 (15) ◽  
pp. 7898
Author(s):  
Grigorios Christidis ◽  
Ersin Karatayli ◽  
Rabea A. Hall ◽  
Susanne N. Weber ◽  
Matthias C. Reichert ◽  
...  
Keyword(s):  
Bile Acid ◽  
Growth Factor ◽  
Liver Injury ◽  
Fibroblast Growth Factor ◽  
Acid Metabolism ◽  
Regulatory Mechanism ◽  
Chronic Liver ◽  
Bile Acid Metabolism ◽  
Fibroblast Growth ◽  
Chronic Liver Injury

Background and Aims: Fibroblast growth factor (FGF) 21 has recently been shown to play a potential role in bile acid metabolism. We aimed to investigate the FGF21 response in an ethanol-induced acute-on-chronic liver injury (ACLI) model in Abcb4−/− mice with deficiency of the hepatobiliary phospholipid transporter. Methods: Total RNA was extracted from wild-type (WT, C57BL/6J) and Abcb4−/− (KO) mice, which were either fed a control diet (WT-Cont and KO-Cont groups; n = 28/group) or ethanol diet, followed by an acute ethanol binge (WT-EtOH and KO-EtOH groups; n = 28/group). A total of 58 human subjects were recruited into the study, including patients with alcohol-associated liver disease (AALD; n = 31) and healthy controls (n = 27). The hepatic and ileal expressions of genes involved in bile acid metabolism, plasma FGF levels, and bile acid and its precursors 7α- and 27-hydroxycholesterol (7α- and 27-OHC) concentrations were determined. Primary mouse hepatocytes were isolated for cell culture experiments. Results: Alcohol feeding significantly induced plasma FGF21 and decreased hepatic Cyp7a1 levels. Hepatic expression levels of Fibroblast growth factor receptor 1 (Fgfr1), Fgfr4, Farnesoid X-activated receptor (Fxr), and Small heterodimer partner (Shp) and plasma FGF15/FGF19 levels did not differ with alcohol challenge. Exogenous FGF21 treatment suppressed Cyp7a1 in a dose-dependent manner in vitro. AALD patients showed markedly higher FGF21 and lower 7α-OHC plasma levels while FGF19 did not differ. Conclusions: The simultaneous upregulation of FGF21 and downregulation of Cyp7a1 expressions upon chronic plus binge alcohol feeding together with the invariant plasma FGF15 and hepatic Shp and Fxr levels suggest the presence of a direct regulatory mechanism of FGF21 on bile acid homeostasis through inhibition of CYP7A1 by an FGF15-independent pathway in this ACLI model. Lay Summary: Alcohol challenge results in the upregulation of FGF21 and repression of Cyp7a1 expressions while circulating FGF15 and hepatic Shp and Fxr levels remain constant both in healthy and pre-injured livers, suggesting the presence of an alternative FGF15-independent regulatory mechanism of FGF21 on bile acid homeostasis through the inhibition of Cyp7a1.

scholarly journals Gut Dysbiosis and Abnormal Bile Acid Metabolism in Colitis-Associated Cancer

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Li Liu ◽  
Min Yang ◽  
Wenxiao Dong ◽  
Tianyu Liu ◽  
Xueli Song ◽  
...  
Keyword(s):  
Bile Acid ◽  
Gut Microbiota ◽  
Bile Acids ◽  
Acid Metabolism ◽  
Farnesoid X Receptor ◽  
Mucosal Barrier ◽  
Bile Acid Metabolism ◽  
Preventive Strategy ◽  
Gut Dysbiosis ◽  
Bile Acid Receptors

Background. Patients with prolonged inflammatory bowel disease (IBD) can develop into colorectal cancer (CRC), also called colitis-associated cancer (CAC). Studies have shown the association between gut dysbiosis, abnormal bile acid metabolism, and inflammation process. Here, we aimed to investigate these two factors in the CAC model. Methods. C57BL/6 mice were randomly allocated to two groups: azoxymethane/dextran sodium sulfate (AOM/DSS) and control. The AOM/DSS group received AOM injection followed by DSS drinking water. Intestinal inflammation, mucosal barrier, and bile acid receptors were determined by real-time PCR and immunohistochemistry. Fecal microbiome and bile acids were detected via 16S rRNA sequencing and liquid chromatography-mass spectrometry. Results. The AOM/DSS group exhibited severe mucosal barrier impairment, inflammatory response, and tumor formation. In the CAC model, the richness and biodiversity of gut microbiota were decreased, along with significant alteration of composition. The abundance of pathogens was increased, while the short-chain fatty acids producing bacteria were reduced. Interestingly, Clostridium XlV and Lactobacillus, which might be involved in the bile acid deconjugation, transformation, and desulfation, were significantly decreased. Accordingly, fecal bile acids were decreased, accompanied by reduced transformation of primary to secondary bile acids. Given bile acid receptors, the ileum farnesoid X receptor-fibroblast growth factor 15 (FXR-FGF15) axis was downregulated, while Takeda G-protein receptor 5 (TGR5) was overexpressed in colonic tumor tissues. Conclusion. Gut dysbiosis might alter the metabolism of bile acids and promote CAC, which would provide a potential preventive strategy of CAC by regulating gut microbiota and bile acid metabolism.

scholarly journals Intestinal bile acid receptors are key regulators of glucose homeostasis

2017 ◽  
Vol 76 (3) ◽  
pp. 192-202 ◽  
Author(s):  
Mohamed-Sami Trabelsi ◽  
Sophie Lestavel ◽  
Bart Staels ◽  
Xavier Collet
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Glucose Homeostasis ◽  
Energy Homeostasis ◽  
Acid Metabolism ◽  
Dietary Lipid ◽  
Farnesoid X Receptor ◽  
Bile Acid Metabolism ◽  
Metabolism Regulation ◽  
Bile Acid Receptors

In addition to their well-known function as dietary lipid detergents, bile acids have emerged as important signalling molecules that regulate energy homeostasis. Recent studies have highlighted that disrupted bile acid metabolism is associated with metabolism disorders such as dyslipidaemia, intestinal chronic inflammatory diseases and obesity. In particular, type 2 diabetes (T2D) is associated with quantitative and qualitative modifications in bile acid metabolism. Bile acids bind and modulate the activity of transmembrane and nuclear receptors (NR). Among these receptors, the G-protein-coupled bile acid receptor 1 (TGR5) and the NR farnesoid X receptor (FXR) are implicated in the regulation of bile acid, lipid, glucose and energy homeostasis. The role of these receptors in the intestine in energy metabolism regulation has been recently highlighted. More precisely, recent studies have shown that FXR is important for glucose homeostasis in particular in metabolic disorders such as T2D and obesity. This review highlights the growing importance of the bile acid receptors TGR5 and FXR in the intestine as key regulators of glucose metabolism and their potential as therapeutic targets.

scholarly journals Oleanolic acid alters bile acid metabolism and produces cholestatic liver injury in mice

2013 ◽  
Vol 272 (3) ◽  
pp. 816-824 ◽  
Author(s):  
Jie Liu ◽  
Yuan-Fu Lu ◽  
Youcai Zhang ◽  
Kai Connie Wu ◽  
Fang Fan ◽  
...  
Keyword(s):  
Bile Acid ◽  
Liver Injury ◽  
Oleanolic Acid ◽  
Acid Metabolism ◽  
Bile Acid Metabolism ◽  
Cholestatic Liver Injury

Allopurinol Protects Against Cholestatic Liver Injury in Mice Not Through Depletion of Uric Acid

2021 ◽  
Author(s):  
Jing Liu ◽  
Yang Fan ◽  
Hang Yu ◽  
Tong Xu ◽  
Chunze Zhang ◽  
...  
Keyword(s):  
Uric Acid ◽  
Bile Acid ◽  
Liver Injury ◽  
Liver Diseases ◽  
Acid Metabolism ◽  
Glutathione Depletion ◽  
Bile Acid Metabolism ◽  
New Perspective ◽  
Cholestatic Liver Injury

Abstract Cholestasis is one of the most severe manifestations of liver injury and has limited therapeutic options. Allopurinol (AP), an inhibitor of uric acid (UA) synthesis, was reported to prevent liver damage in several liver diseases. However, whether AP protects against intrahepatic cholestatic liver injury and what is the role of UA in the pathogenesis of cholestasis remain unknown. In this study, we reported that AP attenuated liver injury in a mouse model of intrahepatic cholestasis induced by alpha-naphthylisothiocyanate (ANIT). AP showed no significant effect on glutathione depletion, inflammation, or bile acid metabolism in livers of ANIT-treated mice. Instead, AP significantly improved fatty acid β-oxidation in livers of ANIT-treated mice, which was associated with activation of PPARα. The protective effect of AP on cholestatic liver injury was not attributable to the depletion of UA, because both exogenous and endogenous UA prevented liver injury in ANIT-treated mice via inhibition of NF-kB-mediated inflammation. In conclusion, the present study provides a new perspective for the therapeutic use of AP and the role of UA in cholestatic liver injury.

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