Document Detail


The role of G-protein-coupled receptors in mediating the effect of fatty acids on inflammation and insulin sensitivity.
MedLine Citation:
PMID:  21587066     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: Chronic activation of inflammatory pathways mediates the pathogenesis of insulin resistance, and the macrophage/adipocyte nexus provides a key mechanism underlying decreased insulin sensitivity. Free fatty acids are important in the pathogenesis of insulin resistance, although their precise mechanisms of action have yet to be fully elucidated. Recently, a family of G-protein-coupled receptors has been identified that exhibits high affinity for fatty acids. This review summarizes recent findings on six of these receptors, their ligands, and their potential physiological functions in vivo.
RECENT FINDINGS: Upon activation, the free fatty acid receptors affect inflammation, glucose metabolism, and insulin sensitivity. Genetic deletion of GPR40 and GPR41, receptors for long-chain and short-chain fatty acids, respectively, results in resistance to diet-induced obesity. Deletion of GPR43 and GPR84 exacerbates inflammation, and deletion of the long-chain fatty acid receptors GPR119 and GPR120 reduces or is predicted to reduce glucose tolerance.
SUMMARY: These studies provide a new understanding of the general biology of gastric motility and also shed valuable insight into some potentially beneficial therapeutic targets. Furthermore, highly selective agonists or antagonists for the free fatty acid receptors have been developed and look promising for treating various metabolic diseases.
Authors:
Da Young Oh; William S Lagakos
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Current opinion in clinical nutrition and metabolic care     Volume:  14     ISSN:  1473-6519     ISO Abbreviation:  Curr Opin Clin Nutr Metab Care     Publication Date:  2011 Jul 
Date Detail:
Created Date:  2011-06-10     Completed Date:  2011-10-06     Revised Date:  2012-02-06    
Medline Journal Info:
Nlm Unique ID:  9804399     Medline TA:  Curr Opin Clin Nutr Metab Care     Country:  England    
Other Details:
Languages:  eng     Pagination:  322-7     Citation Subset:  IM    
Affiliation:
Division of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, California 92093, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Anti-Inflammatory Agents / pharmacology
Cytokines / secretion
Fatty Acid-Binding Proteins / metabolism
Fatty Acids, Nonesterified / pharmacology*
Fatty Acids, Omega-3 / pharmacology
Gene Deletion
Glucose Intolerance / genetics,  metabolism
Humans
Inflammation / genetics,  pathology*
Insulin / secretion
Insulin Resistance*
Intestinal Absorption
Macrophages / metabolism
Mice
Obesity / pathology
Receptors, G-Protein-Coupled / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
P30 DK063491/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Cytokines; 0/Fatty Acid-Binding Proteins; 0/Fatty Acids, Nonesterified; 0/Fatty Acids, Omega-3; 0/Insulin; 0/Receptors, G-Protein-Coupled

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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