Document Detail


Bile acids and insulin resistance: implications for treating nonalcoholic fatty liver disease.
MedLine Citation:
PMID:  19426389     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nonalcoholic fatty liver disease is characterized by an accumulation of excess triglycerides in hepatocytes, and insulin resistance is now considered the fundamental operative mechanism throughout the prevalence and progression of the disease. Besides their role in dietary lipid absorption and cholesterol homeostasis, evidence has accumulated that bile acids are also signaling molecules that play two important roles in glucose and lipid metabolism: in the nuclear hormone receptors as farnesoid X receptors (FXR), as well as ligands for G-protein-coupled receptors TGR5. The activated FXR-SHP pathway regulates the enterohepatic recycling and biosynthesis of bile acids and underlies the down-regulation of hepatic fatty acid and triglyceride biosynthesis and very low density lipoprotein production mediated by sterol-regulatory element-binding protein-1c. The bile acid-TGR5-cAMP-D2 signaling pathway in human skeletal muscle in the fasting-feeding cycle increases energy expenditure and prevents obesity. Therefore, a molecular basis has been provided for a link between bile acids, lipid metabolism and glucose homeostasis, which can open novel pharmacological approaches against insulin resistance and nonalcoholic fatty liver disease.
Authors:
Jue Wei; De Kai Qiu; Xiong Ma
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of digestive diseases     Volume:  10     ISSN:  1751-2980     ISO Abbreviation:  J Dig Dis     Publication Date:  2009 May 
Date Detail:
Created Date:  2009-05-11     Completed Date:  2009-07-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101302699     Medline TA:  J Dig Dis     Country:  Australia    
Other Details:
Languages:  eng     Pagination:  85-90     Citation Subset:  IM    
Affiliation:
Department of Gastroenterology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai Institute of Digestive Disease, Shanghai, China.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bile Acids and Salts / physiology*,  therapeutic use
DNA-Binding Proteins / physiology
Fatty Liver / drug therapy*,  metabolism
Glucose / metabolism
Humans
Insulin Resistance*
Lipid Metabolism
Receptors, Cytoplasmic and Nuclear / physiology
Receptors, G-Protein-Coupled / physiology
Signal Transduction
Transcription Factors / physiology
Chemical
Reg. No./Substance:
0/Bile Acids and Salts; 0/DNA-Binding Proteins; 0/GPBAR1 protein, human; 0/Receptors, Cytoplasmic and Nuclear; 0/Receptors, G-Protein-Coupled; 0/Transcription Factors; 0/farnesoid X-activated receptor; 50-99-7/Glucose

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