In an experiment with unOCN-treated obese mice, OCN improved insulin resistance by decreasing inflammation and increasing insulin signaling and the expression of Slc2a4/GLUT4 in WAT.115 Another study demonstrated that Gprc6a in OCN-mediated activation up-regulated T cell factor 7 (TCF7) expression and its downstream target expression in BAT.116 Activated TCF7 also enhanced Gprc6a and uncoupling protein 1 (UCP1) expression, a core molecule for uncoupling respiration from ATP synthesis in the mitochondria and core molecular for BAT thermogenesis.116. The gene discussed is SLC2A4; the disease is Insulin resistance.