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. 2016 Apr 5;310(11):E900–E911. doi: 10.1152/ajpendo.00328.2015

Fig. 1.

Fig. 1.

Deletion of Bmal1 in white adipose tissue (WAT) and liver of 13- to 24-wk-old female mice on standard rodent chow. Hour 0 represents the beginning of lights-on; n = 3–9/group. A: Bmal1 expression in WAT, genotype F(2, 49) = 18.23, P < 0.0001; time F(5, 49) = 29.76, P < 0.0001; interaction F(10, 49) = 6.604, P < 0.0001, and in liver, genotype F(2, 55) = 8.709, P = 0.0005; time F(5, 55) = 22.75, P < 0.0001; interaction F(10, 55) = 1.860, P = 0.0714. B: Western blot and densitometry analyses of BMAL1 in WAT of mice negative or positive for the aP2-Cre transgene; T = 4.944, DF = 6, and P = 0.0026, and in liver of mice injected with Ad-empty or Ad-Cre virus T = 7.732, DF = 6, and P = 0.0002 at hour 0. C: Dbp expression in WAT, genotype F(2, 49) = 2.481, P = 0.0941; time F(5, 49) = 6.358, P = 0.0001; interaction F(10, 49) = 2.223, P = 0.0317, and in liver, genotype F(2, 55) = 0.9127, P = 0.4075; time F(5, 55) = 11.35, P < 0.0001; interaction F(10, 55) = 1.874, P = 0.0695. *P < 0.05, comparison between control and adipose-Bmal1 knockout (ABKO); #P < 0.05, comparison between control and liver- and adipose-Bmal1 knockout (LABKO); +P < 0.05, comparison between ABKO and LABKO for A and C; ** and ##P < 0.01; *** and ###P < 0.001, **** and ####P < 0.0001.