Extended Data Fig. 3: Cdo1AKO impairs EE and insulin sensitivity in HFD-fed mice.
From: Cdo1 promotes PPARγ-mediated adipose tissue lipolysis in male mice
Mice were treated as indicated in Fig. 3. a: Quantification of adipocyte diameter of BAT in Fig. 3e (n = 6 mice). b-i, Metabolic cage data in the Cdo1AKO or WT mice which were fed on HFD for 4 weeks, n = 7 mice. b: Oxygen consumption rates (VO2) of WT and Cdo1AKO mice, n = 7 mice. c: Regression-based analysis of absolute VO2 against body weight, n = 7 mice. d: Heat production of WT and Cdo1AKO mice, n = 7 mice. e: Regression-based analysis of absolute heat production against body weight, n = 7 mice. f: Carbon dioxide emission (VCO2) of WT and Cdo1AKO mice, n = 7 mice. g: Regression-based analysis of absolute (VCO2) against body weight, n = 7 mice. h:Respiratory Exchange Ratio (RER) in WT and Cdo1AKO mice (n = 7 mice). i: Food intake of the mice (n = 7 mice). j-k: Representative western blot analysis for AKT and its phosphorylation form (p-AKT, s473) (j) and gray scale of p-AKT/AKT (k) in iWAT and liver of WT and Cdo1AKO mice fed with HFD for 2 weeks (n = 3 mice). HSP90-1 is the loading control for p-AKT; HSP90-2 is the loading control for AKT. Mice were administered with insulin for 20 min, after which they were sacrificed and the tissues were harvested for analysis. For statistical analysis, two-way analysis of variance was perfoed in b, d and f. Two-sided ANCOVA analysis was performed in c, e and g. Unpaired two-tailed Student’s tests were performed in a, h, i and k. All data show the means ± SD. Data were compared between WT group and Cdo1AKO group.
