Fig. 2: APOO KO mice exhibited an obesity-prone phenotype with a defect in thermogenesis.
From: Apolipoprotein O modulates cholesterol metabolism via NRF2/CYB5R3 independent of LDL receptor
A–I Eight-week-old male Apoo−/− and Apoo+/+ controls were randomly grouped and fed an NCD (n = 7–8) or HFD (n = 8) for 12 weeks. A Body weights, B Representative images of mice after 12 weeks of NCD or HFD, C Liver/body weight ratios, D Cholesterol content in the livers, E Left: representative hematoxylin and eosin (H&E) and Masson staining of the liver sections of HFD-fed mice, scale bar = 50 μm, boxed regions are shown at a higher magnification; right: quantification of the fibrous area from Masson staining (n = 7), F serum ALT levels of HFD-fed mice, G Left: representative H&E-stained images of WAT of mice in the indicated groups. Scale bar = 50 μm. Right: quantification of adipocyte area, left: the blood glucose levels during the GTT (H) and ITT (I) performed on mice in the indicated groups; right: the Area Under the Curve (AUC) of GTT (H) or ITT (I). Metabolic parameters such as oxygen consumption (VO2) (J), CO2 production (VCO2) (K), and energy expenditure (L) were measured in 10-week-old NCD-fed male mice (n = 8). Values are provided as mean ± SEM. Two-way ANOVA (A, C, D, G–I, L), unpaired two-tailed Student’s t-test (E, F, J, K). *p < 0.05, **p < 0.01, ***p < 0.001. NCD normal chow diet, ANOVA analysis of variance, SEM standard error of the mean, APOO apolipoprotein O, HCD high cholesterol diet, WAT white adipose tissue, GTT glucose-tolerance tests, ITT insulin-tolerance tests.
