Bile Acid Nuclear Receptor Farnesoid X Receptor: Therapeutic Target for Nonalcoholic Fatty Liver Disease.
10.3803/EnM.2016.31.4.500
- Author:
Sun Gi KIM
1
;
Byung Kwon KIM
;
Kyumin KIM
;
Sungsoon FANG
Author Information
1. Department of Integrative Biosciences and Biotechnology, College of Life Sciences, Sejong University, Seoul, Korea. sfang@sejong.ac.kr
- Publication Type:Review
- Keywords:
Bile acids and salts;
Receptors, cytoplasmic and nuclear;
Farnesoid X receptor;
Non-alcoholic fatty liver disease;
Obeticholic acid
- MeSH:
Alcohol Drinking;
Bile Acids and Salts;
Bile*;
Cardiovascular Diseases;
Fatty Liver;
Fibrosis;
Heart Failure;
Hepatocytes;
Inflammation;
Insulin Resistance;
Liver;
Metabolism;
Non-alcoholic Fatty Liver Disease*;
Obesity;
Pathology;
Receptors, Cytoplasmic and Nuclear;
Risk Factors
- From:Endocrinology and Metabolism
2016;31(4):500-504
- CountryRepublic of Korea
- Language:English
-
Abstract:
Nonalcoholic fatty liver disease (NAFLD) is one of the causes of fatty liver, occurring when fat is accumulated in the liver without alcohol consumption. NAFLD is the most common liver disorder in advanced countries. NAFLD is a spectrum of pathology involving hepatic steatosis with/without inflammation and nonalcoholic steatohepatitis with accumulation of hepatocyte damage and hepatic fibrosis. Recent studies have revealed that NAFLD results in the progression of cryptogenic cirrhosis that leads to hepatocarcinoma and cardiovascular diseases such as heart failure. The main causes of NAFLD have not been revealed yet, metabolic syndromes including obesity and insulin resistance are widely accepted for the critical risk factors for the pathogenesis of NAFLD. Nuclear receptors (NRs) are transcriptional factors that sense environmental or hormonal signals and regulate expression of genes, involved in cellular growth, development, and metabolism. Several NRs have been reported to regulate genes involved in energy and xenobiotic metabolism and inflammation. Among various NRs, farnesoid X receptor (FXR) is abundantly expressed in the liver and a key regulator to control various metabolic processes in the liver. Recent studies have shown that NAFLD is associated with inappropriate function of FXR. The impact of FXR transcriptional activity in NAFLD is likely to be potential therapeutic strategy, but still requires to elucidate underlying potent therapeutic mechanisms of FXR for the treatment of NAFLD. This article will focus the physiological roles of FXR and establish the correlation between FXR transcriptional activity and the pathogenesis of NAFLD.
