Fig. 4 |. Specific depletion of JunB in UCP1⁺ adipocyte ( JunB BKO) enhances energy expenditure and protects against diet-induced obesity and insulin resistance.

Six-week-old male JunB BKO and control mice were fed with an HFD for 16 weeks for the following studies. a, JunB deficiency in UCP1⁺ cells protected against HFD-induced obesity. b, JunB BKO mice displayed decreased body mass, fat mass and fat percentage compared to control littermates after HFD feeding. The lean mass, fat mass, total mass and fat percentage were measured using dual-energy X-ray absorptiometry (n = 12, control; n = 11, BKO). c, The mass of gWAT, iWAT, BAT and liver was reduced by JunB deficiency after HFD feeding. The organs were weighed after mice were euthanized (n = 11, control; n = 8, BKO). d, Representative images of gWAT, iWAT, BAT and liver in JunB BKO and control mice. e, H&E staining of gWAT, iWAT and BAT of HFD-fed JunB BKO and control mice. f, Quantification of fat cell size of HFD-fed JunB BKO and control mice in e (n = 6 per group). g,h, Depletion of JunB in UCP1⁺ adipocytes improved glucose tolerance (n = 12, control; n = 11, BKO) (g) and insulin tolerance (n = 12, control; n = 11, BKO) (h). i, JunB BKO mice displayed improved diet-induced hepatic steatosis and fatty liver as reflected in the H&E staining and Bodipy/DAPI immunofluorescence staining. j, Quantification of lipid droplet area in the liver in i (n = 6 per group). Data in a and f-h were analysed by ANOVA. Data in b, c and j were analysed using an unpaired two-sided t-test. Data are presented as the mean ± s.e.m. *P < 0.05; **P < 0.01.