Research Paper Volume 1, Issue 4 pp 425—437

Figure 7. NAC treatment of Atg7 deficient mice prevents the development of a glucose intolerance phenotype. (A) Male Atg7^F/+:Rip2-Cre (n=6 mice), Atg7^F/+:Rip2-Cre (+NAC; n=6 mice), Atg7^F/F:Rip2-Cre (n=11 mice) or Atg7^F/F:Rip2-Cre (+NAC; n=11 mice) were fasted overnight and subsequently injected with 1 g/kg D-glucose. Serum glucose levels were measured and the untreated β cell Atg7 deficient mice were found to be statistically different at the indicated time points, while the other three groups of mice were statistically indistinguishable over the 2 hr timecourse. (B) Insulin levels were determined by tail vein blood sampling at time 0 and 15 min following glucose administration: Atg7^F/+:Rip2-Cre (n=6 mice), Atg7^F/+:Rip2-Cre (+NAC; n=4 mice), Atg7^F/F:Rip2-Cre (n=8 mice) or Atg7^F/F:Rip2-Cre (+NAC; n=5 mice). Data are represented as the mean +/- SEM. * p≤0.05; ** p≤0.001.