Fig. 3.

TGR5 activation induces scWAT beiging at thermoneutrality. a Body weight gain of TGR5 wild-type (Tgr5^+/+) and germline TGR5 knockout (Tgr5^−/−) mice housed at thermoneutrality (30 °C) and subjected to a daily administration of the selective TGR5 agonist INT-777 or vehicle for 7 days. n = 10 per group. b scWAT over body weight (BW) ratio of the mice described in a. c, d mRNA levels of beige remodelling markers Ucp1 and Cidea (c), Pgc1a, Tbx1, Prdm16, and Cd137, Pparg2 and Cebpb; Tgr5 and adrenergic related genes (Adrb3 and Th) (d) in the scWAT of mice described in a. e Representative (n = 10 per group) western blot of PGC-1α, the mitochondrial marker VDAC1, and beiging markers TBX1 and UCP1 from the scWAT of mice described in a. GAPDH was used as loading control. f Representative (n = 5 per group) UCP1 immunostaining of scWAT sections from mice described in a. Scale bars = 50 μm. Results represent mean ± SEM. *P ≤ 0.05, **P ≤ 0.01 and ***P ≤ 0.001 vs. Tgr5^+/+ + Vehicle group by one-way ANOVA followed by Bonferroni post hoc test. Uncropped western blots are provided in Supplementary Fig. 11A–D