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. 2024 Apr 21;84:101945. doi: 10.1016/j.molmet.2024.101945

Figure 4.

Figure 4

The effects of GIP-Cre::hM3Dq activation are maintained in DIO mice. (A) ipgtt (2 g/kg BW glucose, admin of VEH or CNO (at 1 mg/kg ip, delivered contralaterally to glucose at time 0) with AUC (inset) (n = 8 per group). (B) Fast-refeed (as previous) food intake of GIP-Dq mice following treatment with VEH/CNO (at 1 mg/kg BW ip, n = 7–8 per group). (C) Blood glucose in ad lib fed state following treatment with VEH/CNO (n = 7–8 per group). (D) Food intake (interaction F(2,56) = 6.432, p = 0.0031. Post hoc p = 0.0221), (E) Total meal duration (F) Inter-meal interval (treatment F(1,28) = 4.478, p = 0.0434. Post hoc p = 0.0436), (G) Cumulative food intake (interaction F(12,336) = 2.026, p = 0.0215), (H) RER (time F(6.486,147) = 4.453, p = 0.0002), (I) Ambulatory activity (time F(5.666,132.7) = 7.531, p < 0.0001) and (J,K) Energy expenditure (time F(4,692,109.5) = 21.30, p < 0.0001) of GIP-Dq mice treated with VEH/CNO at the onset of the dark phase in ad lib fed animals (n = 15 per treatment). (L) Plasma GIP, (M) Body weight (interaction F(7,91) = 6.117 p < 0.0001), (N) Body weight change (interaction F(7,78) = 2.435, p = 0.0261, treatment F(1,13) = 23.30, p = 0.0003, time F(2.596, 28.93) = 10.74, p = 0.0001) and (O) Cumulative food intake (treatment F(1,13) = 25.65, p = 0.0002), time F(1.607,20.89) = 443.8, p < 0.0001) of GIP-Dq mice treated chronically with DCZ via drinking water (n = 7–8 per group). Values are presented as group mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 by Students T test (A,B(inset)C, D) and two-way ANOVA (D-J, L-N) and ANCOVA (body weight as covariate, K).