Crosstalk between FXR and TGR5 controls glucagon-like peptide 1 secretion to maintain glycemic homeostasis.
10.5625/lar.2018.34.4.140
- Author:
Hyeonhui KIM
1
;
Sungsoon FANG
Author Information
1. Severance Biomedical Science Institute, BK21 PLUS project for Medical Science, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea. sfang@yuhs.ac
- Publication Type:Review
- Keywords:
Bile acids;
Farnesoid X receptor;
G protein-coupled bile acid receptor;
Glucagon-like peptide 1;
obesity;
diabetes
- MeSH:
Bile;
Bile Acids and Salts;
Biological Processes;
Energy Metabolism;
Enteroendocrine Cells;
Glucagon-Like Peptide 1*;
Glucose;
Homeostasis*;
Humans;
Hyperglycemia;
Hyperlipidemias;
Insulin;
Insulin Resistance;
Metabolic Diseases;
Metabolism;
Obesity
- From:Laboratory Animal Research
2018;34(4):140-146
- CountryRepublic of Korea
- Language:English
-
Abstract:
Though bile acids have been well known as digestive juice, recent studies have demonstrated that bile acids bind to their endogenous receptors, including Farnesoid X receptor (FXR) and G protein-coupled bile acid receptor 1 (GPBAR1; TGR5) and serve as hormone to control various biological processes, including cholesterol/bile acid metabolism, glucose/lipid metabolism, immune responses, and energy metabolism. Deficiency of those bile acid receptors has been reported to induce diverse metabolic syndromes such as obesity, hyperlipidemia, hyperglycemia, and insulin resistance. As consistent, numerous studies have reported alteration of bile acid signaling pathways in type II diabetes patients. Interestingly, bile acids have shown to activate TGR5 in intestinal L cells and enhance secretion of glucagon-like peptide 1 (GLP-1) to potentiate insulin secretion in response to glucose. Moreover, FXR has been shown to crosstalk with TGR5 to control GLP-1 secretion. Altogether, bile acid receptors, FXR and TGR5 are potent therapeutic targets for the treatment of metabolic diseases, including type II diabetes.
