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. 2021 Apr 6;33(4):833–844.e5. doi: 10.1016/j.cmet.2021.01.015

Figure 2.

Figure 2

Humanized (h)GIPR knockin mice with conditional CNS-specific hGIPR deletion are protected from diet-induced obesity and glucose intolerance

(A–D) Body weight (A), body composition (B and C), and food intake (D) in male C57BL/6N WT and CNS-hGIPR KO mice (N = 6–8 mice each group).

(E) Hypothalamic expression of proopiomelanocortin (Pomc), brain-derived neurotrophic factor (Bdnf), cocaine-and-amphetamine-regulated transcript (Cart), agouti-related peptide (Agrp), and neuropeptide y (Npy) in 20-week-old male mice (N = 6–7 mice each group).

(F and G) Energy expenditure (F) and locomotor activity (G) in 20-week-old male mice (N = 6 mice each group).

(H–P) Intraperitoneal glucose tolerance (H) and fasting levels of blood glucose (I), insulin (J), GLP-1 (K), leptin (L), triglycerides (M), free fatty acids (N), GIP (O), and cholesterol (P) in WT and CNS-hGIPR KO mice (N = 6–8 mice each group).

(Q) H&E staining of hepatic lipid accumulation (scale bar represents 100 μm).

Data represent means ± SEM. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. Longitudinal data (A and H) were analyzed using two-way ANOVA with time and genotype as co-variables and Bonferroni post hoc analysis for individual time points. Bar graphs (B–E and G–P) were analyzed using two-tailed, two-sided t test. Data in (F) were analyzed using ANCOVA with body weight as co-variate.