Fig. 4.

MiR-21 modulates DHT-mediated changes in BAT adaptive thermogenesis targets. WT or miR21KO mice were treated with dihydrotestosterone (DHT) or vehicle (Veh) for 90 days. Cidea (A), Ppargc1a (B), and Prdm16 (C), Ucp-1 (E), Cpt1a (G), Cpt1b (I), Dio2 (K), Elovl3 (M), and Cox subunits (4i1, 4i2, 7a, and 8b) (O) mRNA was quantified by RT-qPCR and standardized to the geometric mean of four reference genes (HGMK) (N = 6/group). CIDE-A (B), UCP-1 (F), CPT1A (H), CPT1B (J), DIO2 (L), and COX4 (N) proteins were quantified by Western-blot and normalized to GAPDH (N = 4 mice /group). Data are expressed as mean ± SEM. Data were analyzed by two-way ANOVA followed by Fisher’s LSD test. *p < 0.05; **p < 0.01; ****p < 0.0001. CPT1 carnitine palmitoyltransferase 1, COX cytochrome oxidase C, DIO2 deiodinase 2