The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 13 No. 5 • October 2010

Omega-3 Fatty Acids and Inflammation, Insulin-Sensitivity, Fatty Liver

Newly Discovered Receptor for Omega-3 Fatty Acids Mediates Potent
Anti-Inflammatory and Insulin- Sensitizing Effects

The Sept. 3, 2010 Cell1 contained a very exciting paper that reports the discovery that a receptor (GPR120, formerly an orphan receptor), when stimulated by omega-3 fatty acids (DHA and EPA) and palmitoleic acid (found in especially large amounts in macadamia nut oil), causes broad anti-inflammatory effects in immune system cells (RAW 264.7 monocytes and primary intraperitoneal macrophages). Chronic inflammatory effects due to infiltrating macrophages in adipose tissue is a major cause of insulin resistance. 2 When obese mice were fed a high fat diet with omega-3 fatty acids, the fatty acid treatment inhibited inflammation and enhanced systemic insulin sensitivity. But the same omega-3 fatty acid treatment had no such effect in mice whose GPR120 receptor had been knocked out, demonstrating that the effect is mediated by the GPR120 receptor.

The researchers found that stimulation of GPR120 inhibits both TLR4 (toll-like receptor 4)- and TNF-alpha (tumor necrosis factor-alpha) mediated inflammatory responses, thus showing that omega-3 fatty acids can modulate these powerful immune system inflammatory signaling molecules. Also, importantly, GPR120 stimulation by omega-3 fatty acids in wild type mice resulted in a decrease in macrophage proinflammatory genes (M1 type) and an increase in macrophage anti-inflammatory (M2 type) gene expression in adipose tissue. Chronic inflammation in adipose tissue is associated with many complications resulting from diabetes and obesity, such as cardiovascular disease, as well as being a causative factor in aging. 3

Reversal of Fatty Liver by Omega-3 Fatty Acids

The authors also did an in detail lipidomic analysis of fatty acids in the liver and found that the high fat diet-induced increases in triglycerides, diacyglycerol, total saturated fatty acids, and omega-6 fatty acids in the liver were all ameliorated by omega-3 fatty acid treatment and suggest that, “these results are consistent with the view that the reversal of steatosis/non- alcoholic fatty liver disease (NAFLD) by w-3 FA treatment is mediated, in large part, by GPR120 and that the GPR120 KO [knockout] mice are predisposed toward NAFLD even in the context of w-3 FA supplementation.”

We each take 2 capsules four times a day of our omega-3 EPA and DHA supplement. (See "Protect and Enhance Hearts and Minds” in the September 2010 issue of Life Enhancement).


  1. Oh et al. GPR120 is an omega-3 fatty acid receptor mediating potent anti-inflammatory and insulin-sensitizing effects. Cell 142:687-698 (2010).
  2. Nguyen et al. A subpopulation of macrophages infiltrates hypertrophic adipose tissue and is activated by free fatty acids via toll-like receptors 2 and 4 and JNK-dependent pathways. J Biol Chem 282(48):35279-35292 (2007).
  3. Crimmins and Finch. Infection, inflammation, height, and longevity. Proc Natl Acad Sci USA 103(2):498-503 (2006).

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