Blocking the production of TH abrogates the beneficial effects of UA on thermogenesis and body weight control.
(A) Schematic diagram of mice treatment. UA- and vehicle-treated mice were given PTU (8.5 mg/100 ml in the drinking water), an inhibitor of TH synthesis, for a period of 7-week HFD feeding. (B) Body weight time course (n = 6). (C) Daily food intake (n = 6). Weight of (D) total fat mass, (E) BAT, and (F) iWAT (n = 6). (G) GTT and (H) ITT performed in mice (n = 6). (I) Body temperature in mice placed at 21°C (n = 6). mRNA expression of thermogenic genes in (J) BAT and (K) iWAT (n = 6). Immunoblot of UCP-1 and PGC-1α protein in (L) BAT and (M) iWAT (n = 3). C+: positive control from BAT. The underlying data for this figure can be found in S1 Data. BAT, brown adipose tissue; Cidea, Cell death inducing DFFA like effector a; Cox7a1, Cytochrome c oxidase subunit 7a1; Dio2, Deiodinase 2; GTT, glucose tolerance test; HFD, high-fat diet; ITT, insulin tolerance test; iWAT, inguinal white adipose tissue; Pgc1-α, Peroxisome proliferator-activated receptor gamma coactivator 1α; PTU, propylthiouracil; TH, thyroid hormone; UA, urolithin A; UCP-1, Uncoupling protein 1.