Oh Y, Talukdar S, Bae EJ, et al. GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent Anti-inflammatory and Insulin-Sensitizing Effects. Cell 2010 Sep 3;142(5):687-698.
PMID: 20813258
DOI: 10.1016/j.cell.2010.07.041
http://www.cell.com/retrieve/pii/S0092867410008883
http://download.cell.com/pdf/PIIS0092867410008883.pdf?intermediate=true
press coverage : http://www.sciencedaily.com/releases/2010/09/100902121049.htm
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GPR120 Is an Omega-3 Fatty Acid Receptor Mediating Potent Anti-inflammatory and Insulin-Sensitizing Effects
Cell, Volume 142, Issue 5, 687-698, 3 September 2010
Copyright 
2010 Elsevier Inc. All rights reserved.
10.1016/j.cell.2010.07.041
Authors
- Highlights
- GPR120 is expressed in macrophages and Kupffer cells and is induced in obesity
- GPR120 functions as an omega 3 fatty acid (
-3 FA) receptor/sensor - -3 FAs exert broad anti-inflammatory effects through GPR120 in macrophages
- GP120 mediates insulin sensitization by -3 FAs in obese mice
Summary
Omega-3 fatty acids (-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 -3 FA receptor/sensor. Stimulation of GPR120 with -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 -3 FA supplementation. The -3 FA treatment inhibited inflammation and enhanced systemic insulin sensitivity in WT mice, but was without effect in GPR120knockout mice. In conclusion, GPR120 is a functional -3 FA receptor/sensor and mediates potent insulin sensitizing and antidiabetic effects in vivo by repressing macrophage-induced tissue inflammation.