Korean J Obes.  2016 Dec;25(4):167-175. 10.7570/kjo.2016.25.4.167.

Implications for Farnesoid X Receptor Signaling on Bile Acid Metabolism as a Potential Therapeutic Strategy for Nonalcoholic Fatty Liver Disease

Affiliations
  • 1Medical Research Institute, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. cydoctor@chol.com
  • 2Division of Endocrinology and Metabolism, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea.

Abstract

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease in both developed and developing countries and is an important risk factor for both hepatic and cardiometabolic mortality. Despite decades of clinical trials, effective treatment options for NAFLD are limited, requiring novel therapeutic approaches to prevent disease development and progression to cirrhosis and cancer. Recently, bile acids have emerged as signaling molecules and metabolic regulators that can activate signaling mediated by nuclear receptors and G protein-coupled receptors to regulate hepatic lipid, glucose, and energy homeostasis, as well as its own synthesis and transport in the liver and intestine. Many recent studies have reported that the activation or modulation of bile acid signaling mediated by bile acid receptors favorably affects both insulin sensitivity and NAFLD pathogenesis at multiple levels, suggesting that these approaches hold promise as novel therapies. In this review, we provide an overview of the role of bile acids, in particular, their signaling related to the nuclear receptor farnesoid X receptor in NAFLD and new insights into the possible approach of targeting bile acid-related pathways in the treatment of this serious disease.

Keyword

Bile acids; Farnesoid X receptor; Farnesoid X receptor agonists; Gut microbiota; Non-alcoholic fatty liver disease

MeSH Terms

Bile Acids and Salts
Bile*
Developing Countries
Fibrosis
Gastrointestinal Microbiome
Glucose
Homeostasis
Insulin Resistance
Intestines
Liver
Liver Diseases
Metabolism*
Mortality
Non-alcoholic Fatty Liver Disease*
Receptors, Cytoplasmic and Nuclear
Risk Factors
Bile Acids and Salts
Glucose
Receptors, Cytoplasmic and Nuclear
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