Deletion of the Men1 Gene Prevents Streptozotocin-Induced Hyperglycemia in Mice
Figure 4
Tissue specific ablation of floxed Men1 in beta cells increases resistance to STZ-induced hyperglycemia. (a–d) Control and ; RIP-Cre mice at the age of 12 weeks ( to 3 mice) without STZ treatment were sacrificed, and pancreata sections were immunostainined for menin, insulin, or glucagon. (a-b) Immunostaining for menin (red) and insulin (green) in islets in control (a) and ; RIP-Cre mice (b). (c-d) Immunostaining for insulin (green) and glucagon (red) in islets in (c) and ; RIP-Cre mice (d). (e) A schematic of experimental design. Control and ; RIP-Cre mice ( mice) at the age of 12 weeks were injected with STZ at 40 mg/kg of body weight per day for 5 consecutive days. Blood glucose levels were monitored, and mice were sacrificed 4 weeks after STZ injections. (f-g) Immunostaining for menin (red) and insulin (green) in islets in (f) and ; RIP-Cre mice (g) after STZ injections, as described in Figure 4(e). The pancreata were collected 4 weeks after STZ treatment. (h) Non-fasting blood glucose levels before and 4 weeks after STZ injections ( to 15 mice). (i) ; RIP-Cre mice at the age of 12 weeks were injected with STZ at 40 mg/kg of body weight per day for 5 consecutive days. Blood glucose levels in ; RIP-Cre mice before and until 8 weeks after STZ injections ( mice).
