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. 2019 Jan 14;21:22–35. doi: 10.1016/j.molmet.2019.01.002

Figure 2.

Figure 2

Fmr1-deficiency improves glucose tolerance and insulin sensitivity in liver. (A) Glucose tolerance test (GTT) in Fmr1-KO and WT animals. Data are means ± SEM; n = 9 WT, n = 9 KO; 2-way ANOVA: p(Genotype) = 0.0034, p(Time) < 0.0001, p(Interaction) < 0.0001; Šidák's post hoc tests for genotype-wise comparisons: *, p < 0.05, ****, p < 0.0001. (B) Insulin tolerance test (ITT) in Fmr1-KO and WT animals. Data are means ± SEM; n = 8 WT, n = 8 KO; 2-way ANOVA: p(Genotype) = 0.0117, p(Time) < 0.0001, p(Interaction) = 0.0134; Šidák's post hoc tests for genotype-wise comparisons: **, p < 0.01. (C) Cumulative glycemia over the 3 h course of GTT. Data are means ± SEM; n = 9 WT, n = 9 KO; 2-tailed Student's T-test: **, p < 0.01. (D) Cumulative glycemia over the 3 h course of ITT. Data are means ± SEM; n = 8 WT, n = 8 KO; 2-tailed Student's T-test: *, p < 0.05. (E) Western-blot and densitometric analysis of insulin receptor (InsR) and Akt phosphorylation status in liver from Fmr1-KO and WT animals injected with saline or insulin. Densitometric analysis is presented as means ± SEM of phosphoproteins signals ratios relative to total protein, all signals being normalized to β-actin. InsR-Saline: n = 6 animals/group, InsR-Insulin: n = 5 animals/group; 2-way ANOVA: p(Genotype) = 0.0027, p(Treatment) < 0.0001, p(Interaction) = 0.7424; Fisher's LSD post hoc tests for genotype-wise comparisons: *, p < 0.05. Akt: n = 5 animals/group; 2-way ANOVA: p(Genotype) = 0.0215, p(Treatment) < 0.0001, p(Interaction) = 0.0924; Fisher's LSD post hoc tests for genotype-wise comparisons: **, p < 0.01.