A proposed mechanism for the induction of Eprosartan Mesylate apoptosis could be oxidative stress, which is associated with abnormal cell cycle checkpoint function. Under normal circumstances the cell cycle proceeds without interruptions. However, if cycling cells are damaged by agents which induce oxidative stress, a G2 check point response is triggered and cells pause and repair the damage. In the case of a severe damage, cells may alternatively undergo apoptosis. Given the role of AIF in mitochondrial respiration as a hydrogen peroxide scavenger, loss of AIF could result in an accumulation of ROS, which would then generate a misregulation of b-cell cycle and apoptosis. This is further supported by the finding, that b-cells from both AIF-deficient mice and human islets displayed increased sensitive to cell death induced by hydrogen peroxide. b-cells are in general very sensitive to oxidative stress, in particular with hydrogen peroxide, due to their low expression of a peroxide scavenging system. Given the role of b-cell mitochondria as key regulators of glucose stimulated insulin secretion, we hypothesized that Hq mice show an impaired glucose tolerance. Surprisingly, and in accordance to a recent study, AIF deficiency in Hq Azlocillin sodium salt mutant mice did not impair glucose tolerance. Hq mice were rather hypoglycemic compared to wt. This could be due to impaired glucose sensing as a result of selective neuron loss reported in Hq mutant mice, but is more likely to be a result of improved insulin sensitivity. Many studies have linked changes in mitochondrial oxidative phosphorylation to the development of insulin resistance and diabetes: Importantly, a recent study in tissue specific muscle and liver AIF knockout mice and Hq mice with a global AIF deficiency shows that a primary OxPhos defect alone does not cause diabetes, but rather increases insulin sensitivity and reduces fat mass. In line with our results, this study found that Hq mice displayed improved glucose tolerance associated with reduced fasting and glucose-induced insulin secretion, possibly due to the improved insulin sensitivity. This explains, why Hq mice still maintain normoglycemia, despite their loss of b-cell mass.