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

Figure 1.

Figure 1

GIP-Cre::hM3Dq activation significantly improves glucose tolerance. (A) Schematic for the GIP-Dq mouse model. (B) Representative section from the small intestine of GIP-Dq mice demonstrating Dq (green) and DAPI (white) expression. Scale bar – 100um. (C) Plasma GIP of WT mice receiving oral gavage of liquid Ensure, a mixed meal. (D–G) Plasma (D) GIP, (E) insulin, (F) mPYY and (G) total GLP-1 (TGLP-1) of GIP-Dq mice treated with CNO (1 mg/kg BW ip). (H) 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 = 16–24 per group). (I–K) Plasma (I) GIP (one-way ANOVA: effect of treatment F(3,24) = 133.3, p < 0.0001. Post hoc p < 0.0001), (J) insulin (effect of treatment F(3,20) = 10.95, p < 0.0001. Post hoc p = 0.0017) and (K) TGLP-1 (effect of treatment F(3,24) = 1.275, p = 0.3053) at basal and +15 mins post glucose (as previous). Animals were subsequently pre-treated with a GIPR monoclonal antibody antagonist or isotype control antibody 48 h prior to (L) ipgtt (as previous) and (M) AUC (n = 7 per group, effect of treatment F(3,24) = 38.73, p < 0.0001. Post hoc p = 0.0001). Values are presented as group mean ± SEM. ∗p < 0.05, ∗∗∗p < 0.001 and ∗∗∗∗p < 0.0001 by paired students T test (C-H[inset]) and one-way ANOVA (I-K, M[inset]).