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. Author manuscript; available in PMC: 2018 Apr 1.
Published in final edited form as: Neurobiol Dis. 2017 Jan 17;100:87–98. doi: 10.1016/j.nbd.2017.01.004

Figure 3. Diet-induced obesity leads to glucose intolerance to a greater extent in APP/PSEN1 mice and is rescued by reversal to LFD.

Figure 3

Blood glucose: HFD significantly increased fasted blood glucose levels in A) male (F1, 77=68.59, P<0.001) and B) female mice (F1, 73=114.79, P<0.001) following 20 weeks on diet. There were no effects of genotype on this measure (Fs<1.38, Ps>0.24). N=15–29 per group. Glucose tolerance test-9.5 months: In both C) males and D) females Area Under the Curve (AUC) measurements were significantly elevated in APP/PSEN1-HFD mice compared to other groups (Genotype x Diet interaction F1, 27=13.340, P=0.001 and F1, 27=16.343, P=0.001 respectively) indicating that groups responded to the glucose bolus differently. N=5–10 per group. Glucose tolerance test-12 months REV diets completely reversed glucose intolerance phenotype in both WT and APP/PSEN1 mice. E) In males AUC was larger in APP/PSEN1 mice (F1, 41 = 9.592, P=0.004), and in HFD-fed mice (F2, 41 = 37.243, P<0.001), with no interaction among the factors. F) In females the effect of HFD was even greater in APP/PSEN1 mice (F2, 42 = 7.136, P=0.002). N=5–10 per group.

Data were analyzed by 2(genotype) x 2 or 3(diet) ANOVA. *, **, *** P<0.05, 0.01, 0.001 indicates different compared to all other groups, or as marked. For Eii) ## P<0.001, indicates main effect of genotype; +++ P<0.001 indicates main effect of diet, HFD compared to LFD and REV, regardless of genotype.