Fig. 1: TBC, an intestinal selective PXR agonist, ameliorates HFD-induced obesity and insulin resistance.

a, b The mRNA expression of Cyp3a11, a typical target gene of PXR in the liver (a; n = 5 for Veh and PCN, n = 8 for Veh and TBC) and intestine (b; n = 8 for Veh, n = 10 for PCN, n = 7 for Veh and TBC) of WT mice treated with PCN (40 mg/kg) once every 8 hours for three times. c, d The mRNA expression of Cyp3a11 in the liver (c; n = 5 for Veh, n = 3 for PCN, n = 6 for Veh, n = 4 for TBC) and intestine (d; n = 5 for Veh, n = 4 for PCN, n = 7 for Veh and TBC) of PXR knockout mice treated with PCN or TBC. e Appearance (top) and growth curve (bottom) of vehicle (Veh) and TBC-treated mice. WT mice fed with high-fat diet (HFD) supplemented with vehicle or 0.05% TBC for 12 weeks (n = 8 per group). f–h Representative photographs and the ratio of fat depots to body weight of eWAT (f), iWAT (g), and BAT (h) (n = 8 per group). i H&E staining of adipose tissues. Scale bar: 50 μm. j Distribution of adipocyte size of eWAT and iWAT (n = 3 per group). k, l Blood glucose concentrations during GTT (2 g/kg; k) and ITT (0.75 U/kg; l) in vehicle and TBC-treated WT mice (n = 6 for Veh, n = 7 for TBC). m Serum insulin levels of vehicle and TBC treated mice (n = 6 for Veh, n = 8 for TBC). n Serum leptin levels vehicle and TBC treated mice (n = 8 per group). PXR KO PXR whole-body knockout mice, WT wild type, eWAT epididymal white adipose tissue, iWAT inguinal white adipose tissue, BAT brown adipose tissue, GTT glucose tolerance test, ITT insulin tolerance test. Data are mean ± SEM. All the data were assessed form normal distribution before statistical analysis. Significance was analyzed using two-way analysis of variance (ANOVA) with Sidak’s multiple comparisons test (Fig. 1e, k, and l). The remaining statistical differences were determined using unpaired two-tailed Student’s t test. Source data are provided as a Source Data file.