Fig. 3 |. Adipose-specific JunB-deficient ( JunB FKO) mice exhibit enhanced thermogenesis and cold adaptation.

a,b, Expression levels of JunB in protein (n = 3, independent experiments) (a) and mRNA (n = 4 mice per group) (b) in BAT and WAT were notably suppressed by depletion of JunB in adipocytes with little effect on other tissues. Mus, skeletal muscle; Liv, liver; Pan, pancreas; Hyp, hypothalamus; Ctrl, control. c, JunB deficiency enhanced cold-induced oxygen consumption at both light and dark cycles. d, Data analysis of oxygen consumption from c using the CaIR website as described⁶⁴. e, JunB deficiency prevented the decrease in core body temperature under cold stress conditions. f, JunB deficiency induced mRNA expression of mitochondria and thermogenic markers in BAT compared to controls (n = 6 mice per group). g, Depletion of JunB increased the average copy number of mitochondria and the proportion of high-mitochondria cells in BAT (n = 4 per group). LD, lipid droplet; N, nucleus. h, Quantification of mitochondrial number in individual cells from g. i, JunB deficiency significantly increased the ratio of mtDNA/nDNA (n = 8 mice per group). j, Elimination of JunB⁺ adipocytes significantly increased oxygen consumption at both light and dark cycles. k, Analysis of oxygen consumption from j using CaIR. Data in e and h were analysed by analysis of variance (ANOVA). The other data were analysed by unpaired two-sided t-test. Data are presented as the mean ± s.e.m. *P < 0.05 or **P < 0.01.