Document Detail

GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects.
MedLine Citation:
PMID:  20813258     Owner:  NLM     Status:  MEDLINE    
Omega-3 fatty acids (omega-3 FAs), DHA and EPA, exert anti-inflammatory effects, but the mechanisms are poorly understood. Here, we show that the G protein-coupled receptor 120 (GPR120) functions as an omega-3 FA receptor/sensor. Stimulation of GPR120 with omega-3 FAs or a chemical agonist causes broad anti-inflammatory effects in monocytic RAW 264.7 cells and in primary intraperitoneal macrophages. All of these effects are abrogated by GPR120 knockdown. Since chronic macrophage-mediated tissue inflammation is a key mechanism for insulin resistance in obesity, we fed obese WT and GPR120 knockout mice a high-fat diet with or without omega-3 FA supplementation. The omega-3 FA treatment inhibited inflammation and enhanced systemic insulin sensitivity in WT mice, but was without effect in GPR120 knockout mice. In conclusion, GPR120 is a functional omega-3 FA receptor/sensor and mediates potent insulin sensitizing and antidiabetic effects in vivo by repressing macrophage-induced tissue inflammation.
Da Young Oh; Saswata Talukdar; Eun Ju Bae; Takeshi Imamura; Hidetaka Morinaga; WuQiang Fan; Pingping Li; Wendell J Lu; Steven M Watkins; Jerrold M Olefsky
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Cell     Volume:  142     ISSN:  1097-4172     ISO Abbreviation:  Cell     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-03     Completed Date:  2010-09-20     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  0413066     Medline TA:  Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  687-98     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier Inc. All rights reserved.
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MeSH Terms
3T3-L1 Cells
Anti-Inflammatory Agents / administration & dosage,  metabolism
Cell Line
Dietary Fats / metabolism
Dietary Supplements
Fatty Acids, Omega-3 / administration & dosage*,  metabolism*
Hypoglycemic Agents / administration & dosage,  metabolism
Insulin Resistance*
Macrophages / immunology
Mice, Knockout
Obesity / complications
Receptors, G-Protein-Coupled / genetics,  metabolism*
Grant Support
DK 074868/DK/NIDDK NIH HHS; DK033651/DK/NIDDK NIH HHS; DK063491/DK/NIDDK NIH HHS; P01 DK074868/DK/NIDDK NIH HHS; P01 DK074868-02/DK/NIDDK NIH HHS; P01 DK074868-05/DK/NIDDK NIH HHS; P30 DK063491/DK/NIDDK NIH HHS; P30 DK063491-07/DK/NIDDK NIH HHS; R01 DK033651/DK/NIDDK NIH HHS; R37 DK033651/DK/NIDDK NIH HHS; R37 DK033651-26/DK/NIDDK NIH HHS; R37 DK033651-27/DK/NIDDK NIH HHS; U54 HD 012303-25/HD/NICHD NIH HHS; U54 HD012303/HD/NICHD NIH HHS; U54 HD012303-25A1/HD/NICHD NIH HHS; U54 HD012303-28/HD/NICHD NIH HHS
Reg. No./Substance:
0/Anti-Inflammatory Agents; 0/Dietary Fats; 0/Fatty Acids, Omega-3; 0/Hypoglycemic Agents; 0/O3far1 protein, mouse; 0/Receptors, G-Protein-Coupled
Comment In:
Cell. 2010 Sep 3;142(5):672-4   [PMID:  20813253 ]

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

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