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. 2021 Sep 8;6(17):e150249. doi: 10.1172/jci.insight.150249

Figure 6. miR-182-5p overexpression in subcutaneous fat pad of mice resists obesity and its metabolic consequences.

Figure 6

C57BL/6 mice were fed HFD for 8 weeks and then received subcutaneous fat pad injection of miR-182-5p agomir or control agomir (nc-agomir) every 3 days for 8 injections. (A) Representative images of miR-182-5p agomir and nc-agomir mice after a 17-week HFD feeding. (B) Body weight (BW) of miR-182-5p agomir and nc-agomir mice fed with HFD for 17 weeks (n = 4/group). (C) Body composition of HFD-fed miR-182-5p agomir and nc-agomir mice (n = 4/group). (D) Representative images of fat pads from HFD-fed miR-182-5p agomir and nc-agomir mice. (E) Weights of sWAT, eWAT, and BAT of HFD-fed miR-182-5p agomir and nc-agomir mice (n = 4/group). (F) Representative images of hematoxylin and eosin staining of sWAT, eWAT, BAT, and liver sections from HFD-fed miR-182-5p agomir and nc-agomir mice (n = 3 biological replicates; scale bar: 100 μm). Glucose tolerance tests (G) and insulin tolerance tests (H) were performed in HFD-fed miR-182-5p agomir and nc-agomir mice (n = 4–5/group) according to similar procedures as described in our previous studies (32). (I) mRNA levels of thermogenic marker genes in sWAT of HFD-fed miR-182-5p agomir and nc-agomir mice were quantified by qRT-PCR and normalized to β-actin (n = 6/group). (J) A proposed model of the mechanism by which miR-182-5p promotes thermogenic gene expression in white adipocytes. Data represent mean ± SEM. Significance determined by unpaired 2-tailed Student’s t test. *P < 0.05; **P < 0.01.