Fig. 5: THA selectively activates GPR120 to promote adipocyte browning.

a Gene expression of five fatty acid receptors in iWAT of WT mice housed under 30 °C or 4 °C (n = 8). b Schematic representation of Tango (β-arrestin recruitment) assay: (1) Activation of GPCR by agonist. (2) Recruitment of β-arrestin and TEV protease to the C terminus. (3) Cleavage of TEV site leading to the release of the transcription factor tTA. (4) Released tTA induces luciferase expression. Created with BioRender.com. c Tango assay of five fatty acid receptors stimulated by THA (n = 4). d Calcium release assay in 293T cells expressing mouse GPR120 after treatment with GSK137647A, palmitic acid (PA), EPA or THA (n = 4). e Representative images of cell stained with Fluo-4 calcium indicator after treatment with GSK137647A, PA, EPA or THA at 0.2 μM or 20 μM (scale bar, 50 μm). f Gene expression in iWAT adipocytes treated with PA or AH, in the presence of GPR120 inhibitor AH7614 or vehicle (n = 3). g–i Gene expression (g), UCP1 protein levels (h) and OCR (i) of Lenti-Scr or Lenti-shGPR120-infected iWAT adipocytes treated with vehicle or THA; (n = 3 in (g), n = 4 in (h) and n = 11 in (i)). Data in (a, c, d) and (f–i) are from biologically independent samples. Data with error bars are reported as the mean ± SEM. P values were determined by two-sided unpaired Student’s t test in a or two-way ANOVA followed by Fisher’s LSD test in (d), and (f–i). n.s., not significant. Source data are provided as a Source Data file.