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. 2022 Oct 20;23(20):12635. doi: 10.3390/ijms232012635

Figure 2.

Figure 2

dbh-CB1-KO mice show a reduced body weight gain, increased thermogenic markers in BAT, decreased fat mass, and adipogenesis markers in visceral fat. (A) dbh-CB1-KO mice are resistant to HFD-induced obesity compared with WT (n = 15 each). *** p ≤ 0.001 by repeated measures two-way ANOVA. (B) dbh-CB1-KO mice show no differences in food intake (n = 15; Student t-test). (C) dbh-CB1-KO show decreased plasma leptin level (n = 8). ** p ≤ 0.01 by Student t-test. (D) Fasting plasma insulin levels in mice on HFD. (E) Lower plasma triglyceride levels in dbh-CB1-KO mice on HFD. (F) Lower LDL cholesterol levels in dbh-CB1-KO mice on HFD but no differences in HDL cholesterol levels compared with WT mice (n = 7–8). * p ≤ 0.05 by student t-test. (G) HFD-fed dbh-CB1-KO mice show significantly low liver triglyceride tissue levels (n = 4–5). * p ≤ 0.05 by student t-test. Data are expressed as mean ± SE. (H) dbh-CB1-KO show decreased visceral fat (n = 8–9). * p ≤ 0.05 by Student t-test. (I) Hematoxylin and eosin staining on histological sections from visceral fat tissue. Scale bar = 100 μm. (J) Quantitative analysis of adipocyte size (n = 3). ** p ≤ 0.01 by Student t-test. (K) dbh-CB1-KO show decreased Lep, Fas, and Cebpb mRNA levels in visceral fat whereas no significant differences are observed in the other markers of adipogenesis. (L) dbh-CB1-KO show increased Ucp1, Tfam, and Lipe in BAT. For (K,L) (n = 4), * p ≤ 0.05 by Student t-test. Data are expressed as mean ± SE.