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

Figure 3.

Figure 3

Central GIPR antagonism abolishes the effect on food intake but not glucose tolerance. Representative cfos staining of the ARC, AP and NTS of (A) GIP-Dq mice treated with VEH/CNO (at 1 mg/kg BW ip, n = 6 per group) and (B) WT/GIPR-Cre::GCaMP3 mice treated with VEH/[D-Ala2]-GIP; scale bars represent 100 μm and numbers at the top refer to Bregma. (C,D), quantification of conditions shown in a and b, respectively showing average c-Fos positive cells per section. Each point represents data from an individual mouse. (E) Food intake (at the onset of the dark phase) of ad lib fed GIP-Dq mice receiving ICV pre-treatment with IsoAb/GIPR Ab antagonist (n = 4–5 per group, interaction F(6,26) = 7.174, p = 0.0001, time F(1.116,14.51) = 137.5, p < 0.0001, treatment F(1,13) = 9.690, p = 0.0013. Post hoc p = 0.030). (F) Food intake in fast/refeed paradigm (n = 8–11 per group, treatment F(3,30) = 8.765, p = 0.0003. Post hoc p = 0.0019). (G) ipgtt (as previous) and (H) AUC (n = 3–6 per group, treatment F(3,14) = 15.77, p < 0.0001. Post hoc p = 0.0079 and p = 0.0054 respectively). Values are presented as group mean ± SEM. ∗∗p < 0.01 by Students T test (C and D), two-way ANOVA (E) and one-way ANOVA (F, H).