Document Detail


Review article: the emerging interplay among the gastrointestinal tract, bile acids and incretins in the pathogenesis of diabetes and non-alcoholic fatty liver disease.
MedLine Citation:
PMID:  23057494     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Recent research has led to an interest in the role of the gut and liver in type 2 diabetes mellitus (T2DM).
AIM: To review the role of the gastrointestinal system in glucose homoeostasis, with particular focus on the effects of incretin hormones, hepatic steatosis and bile acids.
METHODS: PubMed and Google Scholar were searched using terms such as incretin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), dipeptidyl peptidase-4 (DPP-4), hepatic steatosis, bile acid and gastric bypass. Additional relevant references were identified by reviewing the reference lists of articles.
RESULTS: Perturbations of incretin hormones and bile acid secretion contribute to the pathogenesis of T2DM, leading to their potential as therapeutic targets. The incretin hormones (GIP and GLP-1) are deactivated by DPP-4. GLP-1 agonists and DPP-4 inhibitors improve glycaemic control in patients with T2DM. Hepatic steatosis, along with insulin resistance, may precede the development of T2DM, and may benefit from anti-diabetes medications. Bile acids play an important role in glucose homoeostasis, with effects mediated via the farnesoid X receptor (FXR) and the cell surface receptor TGR5. The bile acid sequestrant colesevelam has been shown to be effective in improving glycaemic control in patients with T2DM. Altered gastrointestinal anatomy after gastric bypass surgery may also affect enterohepatic recirculation of bile acids and contribute to improved glycaemic control.
CONCLUSIONS: Research in recent years has led to new pathways and processes with a role in glucose homoeostasis, and new therapeutic targets and options for type 2 diabetes mellitus.
Authors:
A Zarrinpar; R Loomba
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2012-10-11
Journal Detail:
Title:  Alimentary pharmacology & therapeutics     Volume:  36     ISSN:  1365-2036     ISO Abbreviation:  Aliment. Pharmacol. Ther.     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-10-17     Completed Date:  2013-03-20     Revised Date:  2013-11-06    
Medline Journal Info:
Nlm Unique ID:  8707234     Medline TA:  Aliment Pharmacol Ther     Country:  England    
Other Details:
Languages:  eng     Pagination:  909-21     Citation Subset:  IM    
Copyright Information:
© 2012 Blackwell Publishing Ltd.
Affiliation:
Division of Gastroenterology, Department of Medicine, University of California at San Diego, La Jolla, CA 92093-0063, USA.
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MeSH Terms
Descriptor/Qualifier:
Bile Acids and Salts / metabolism*
Blood Glucose / metabolism*
Diabetes Mellitus, Type 2 / etiology*,  metabolism,  physiopathology
Fatty Liver / etiology*,  metabolism,  physiopathology
Gastric Bypass
Gastrointestinal Tract / metabolism*
Homeostasis
Humans
Incretins / metabolism*
Grant Support
ID/Acronym/Agency:
K23 DK090303/DK/NIDDK NIH HHS; K23 DK090303/DK/NIDDK NIH HHS; T32 DK07202/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Bile Acids and Salts; 0/Blood Glucose; 0/Incretins
Comments/Corrections

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