Animal experiment:

Mice: Male C57Bl/6 WT or Gpr120 KO littermates are fed a normal chow (13.5% fat) or high-fat diet (60% fat) ad libitum for 15-20 weeks from 8 weeks of age. After 15 weeks on HFD, WT and Gpr120 KO mice are switched to an isocaloric HFD supplemented with ω3-FA concentrate or 30 mg/kg GPR120-IN-1 and fed for 5 weeks. Mice receive fresh diet every 3rd day, and food consumption and body weight are monitored[1].

GPR120 Compound A is an orally active and high-affinity agonist of GPR120 [1].

G-protein coupled receptor 120 (GPR120, free fatty acid receptor 4/FFAR4) is a G protein-coupled receptor which has been expressed in intestine, adipocytes, and pro-inflammatory macrophages that is activated by long chain free fatty acids. GPR120 has been involved in mediating the anti-inflammatory and insulin-sensitizing effects of omega 3 fatty acids. Deficiency of GPR120 is responsible for reduced fat metabolism, produce anti-inflammatory effects and to acutely potentiate insulin secretion [2].

GPR120 compound A activated GPR120 with the EC50 value of ~0.35 μM. GPR120 compound A demonstrated potent selectivity over another lipid-sensing G-protein, GPR40 (FFAR1). In a high-fat diet fed obese mice, GPR120 compound A (30 mg/kg) exerted anti-inflammatory effects on macrophages in vitro and improved glucose tolerance, decreased hyperinsulinemia, increased insulin sensitivity, and decreased hepatic steatosis [1].

References:
[1] Walenta E, Akiyama T E, Lagakos W S, et al.  A Gpr120-selective agonist improves insulin resistance and chronic inflammation in obese mice[J]. Nature medicine, 2014, 20(8): 942-947.
[2] Ichimura A, Hirasawa A, Poulain-Godefroy O, et al.  Dysfunction of lipid sensor GPR120 leads to obesity in both mouse and human[J]. Nature, 2012, 483(7389): 350-354.