Fig. 2: Hepatic ACOX1 deficiency promotes basal energy expenditure and browning of subcutaneous white adipose tissue.

a Oxygen consumption rat (VO₂) of HFD-fed control (n = 7) and Acox1-LKO (n = 6) mice. b Analysis of energy expenditure in control and Acox1-LKO mice. c Browning gene expression in iWAT of control and Acox1-LKO mice fed normal chow diet (n = 11). d Western blot analysis of UCP1, Tomm20 and mitochondrial respiratory complex V, III, and II in iWAT from mice after a 2-day cold exposure (n = 3). e UCP1 immunohistochemistry in iWAT from control and Acox1-LKO mice after cold exposure (n = 2; scale bar, 25 μm). f Activities of mitochondrial complex II and complex IV from mice iWAT were measured using Seahorse (n = 10). g VO₂ of control and Acox1-LKO mice before and after CL316,243 injection (n = 7). h Strategy for treatment of adipocytes derived from WT iWAT with serum from Acox1-LKO or control mice. Created with BioRender.com. i Western bolt analysis of UCP1 and COX4 (n = 3). j Browning gene expression in iWAT adipocytes treated with whole or delipidated mouse serum (n = 3). Data in (a–d, f, g, i, and j) are from biologically independent samples. Images in (e) are representative of two separate experiments. Data with error bars are the mean ± SEM. P values were determined by two-sided unpaired Student’s t test in (a) (right panel) and (c), two-way ANOVA with Tukey’s honest difference post hoc test in (a) (left panel), ANCOVA in (b), two-way ANOVA followed by Fisher’s LSD test in (f, g, and j). n.s., not significant. Source data are provided as a Source Data file.