Bile acid receptors in non-alcoholic fatty liver disease.

Title

Bile acid receptors in non-alcoholic fatty liver disease.

Creator

Li Yuanyuan; Jadhav Kavita; Zhang Yanqiao

Publisher

Biochemical pharmacology

Date

2013
2013-12

Description

Accumulating data have shown that bile acids are important cell signaling molecules, which may activate several signaling pathways to regulate biological processes. Bile acids are endogenous ligands for the farnesoid X receptor (FXR) and TGR5, a G-protein coupled receptor. Gain- and loss-of-function studies have demonstrated that both FXR and TGR5 play important roles in regulating lipid and carbohydrate metabolism and inflammatory responses. Importantly, activation of FXR or TGR5 lowers hepatic triglyceride levels and inhibits inflammation. Such properties of FXR or TGR5 have indicated that these two bile acid receptors are ideal targets for treatment of non-alcoholic fatty liver disease, one of the major health concerns worldwide. In this article, we will focus on recent advances on the role of both FXR and TGR5 in regulating hepatic triglyceride metabolism and inflammatory responses under normal and disease conditions.

Subject

Animals; Bile Acids and Salts/*metabolism; Cholesterol; Cytoplasmic and Nuclear/agonists/*metabolism; Fatty Liver/drug therapy/immunology/*metabolism; FXR; G-Protein-Coupled/agonists/*metabolism; Glucose/metabolism; Humans; Inflammation; Lipid Metabolism/drug effects; Lipid Regulating Agents/chemistry/pharmacology/therapeutic use; Molecular Structure; Non-alcoholic Fatty Liver Disease; Receptors; TGR5; Triglyceride; Triglycerides/metabolism

Rights

Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).

Pages

1517–1524

Issue

11

Volume

86

Citation

Li Yuanyuan; Jadhav Kavita; Zhang Yanqiao, “Bile acid receptors in non-alcoholic fatty liver disease.,” NEOMED Bibliography Database, accessed March 28, 2024, https://neomed.omeka.net/items/show/3483.