Fig. 8: B3galt5 mediates the effects of intestinal of PXR activation on obese mice.

WT and B3galt5 KO mice were fed with TBC supplemented in HFD at 0.05% (w/w) for 12 weeks. a Appearance (top) and growth curve (bottom) of vehicle (Veh) and TBC treated WT and B3galt5 KO mice (n = 10 for WT + Veh and WT + TBC, n = 7 for B3galt5-/- + Veh, n = 9 for B3galt5-/- + TBC). b Representative photographs of eWAT, iWAT and BAT (left) and the ratio of fat depots to body weight (right; n = 7–10 as (a)). c, d H&E staining of adipose tissues (c) and distribution of adipocyte size of eWAT and iWAT (d; n = 3 per group). Scale bar: 50 μm. e, f Blood glucose concentrations during GTT (2 g/kg; e) and ITT (1 U/kg; f) in Veh and TBC-treated B3galt5 KO mice (n = 7 for B3galt5-/- + Veh, n = 9 for B3galt5-/- + TBC). g Serum leptin levels in Veh and TBC treated B3galt5 KO mice (n = 7–9 as (e-f)). h Serum insulin levels in Veh and TBC treated B3galt5 KO mice (n = 7–9 as (e–f)). WT wild type; B3galt5-/-: B3galt5 whole-body knockout, TBC tributyl citrate, eWAT epididymal white adipose tissue, iWAT inguinal white adipose tissue, BAT brown adipose tissue. 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. 8a). The remaining statistical differences were determined using unpaired two-tailed Student’s t test. Source data are provided as a Source Data file.