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. 2020 Oct 15;8(1):e001199. doi: 10.1136/bmjdrc-2020-001199

Figure 2.

Figure 2

Impaired glucose uptake in Hap1+/- mice as well as in Hap1-knocked out adipocytes. Hap1+/- and WT mice were fed with ND, and glucometabolic parameters were monitored. (A) Representative images of Hap1+/- (32 g body weight) and WT (26 g) mice at week 40 and kinetics of body weight increase rate of mice (n=6 for Hap1+/- mice and n=4 for WT mice), p<0.001 for genotype effect across all time points (two-way ANOVA). (B) Blood glucose levels of mice fasting for 16 hours at 25 weeks (n=7 for Hap1+/- mice and n=4 for WT mice), p=0.2589. (C) Plasma insulin levels of Hap1+/- ± (n=5 per group), *p<0.05. (D) Relative blood glucose levels and AUC during a GTT at 25 weeks (n=7 for Hap1+/- mice and n=4 for WT mice), p=0.0018 for genotype effect (two-way ANOVA), p=0.012 for genotype and time interaction. (E) Relative blood glucose levels and AUC during an ITT at 25 weeks (n=6 for Hap1+/- mice and n=4 for WT mice), p<0.001 for genotype and time interaction. (F) Glucose consumption in primary Hap1-/- and WT adipocytes after 24-hour insulin stimulation (n=9 per group). (G) The representative images and microplate fluorimeter measurement of 2-NBDG uptake of primary Hap1-/- and WT adipocytes in the absence (0 nM) and presence (100 nM) of insulin for 30 min (scale bar, 20 µm, n=3 per group). Data are presented as mean±SEM. *p<0.05, **p<0.01 and ***p<0.001 (unpaired two-tailed t tests for bar charts; two-way ANOVA with Bonferroni multiple comparisons test for time plots, for Hap1+/- versus WT mice at time point shown). ANOVA, analysis of variance; AUC, area under the curve; GTT, glucose tolerance test; HAP1, huntingtin-associatedprotein 1; INS, insulin; ITT, insulin tolerance test; 2-NBDG, 2-(N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl)Amino)-2-Deoxyglucose; ND, normal diet; WT, wild type.