Induction of the type 2 diabetic mouse model and the effect of LDR on diabetes-induced hyperglycemia, insulin resistance and inactivation of Akt.

<p>The type 2 diabetic mouse model was established by a combination of a HFD and STZ treatment. C57BL/6J mice were fed with a HFD (40% of calories from fat) for 12 weeks to induce obesity (A), which exhibited abnormal blood glucose tolerance (B) and insulin resistance (C). After intraperitoneal injection of STZ (50 mg/kg), the type 2 diabetic mouse model was successfully induced with the characteristic of hyperglycemia (>12 mmol/L, D). The diabetic or control mice were irradiated with LDR at 25, 50, or 75 mGy over whole-body once every other day for the indicated times. The blood glucose levels and insulin tolerance at the 4-week time-point (E, G) and 8-week time-point (F, H) were examined. The <i>t</i>-Akt and <i>p</i>-Akt in kidneys were detected by western blotting assay (I). Data are presented as means ± SEM. n = 9 in diabetic group and n = 8 in each other group. *<i>p</i><0.05 vs. the corresponding control group; #<i>p</i><0.05 vs. the corresponding DM group. Con, control mice; Con/50 mGy, control mice treated with 50 mGy; DM, diabetic mice without LDR treatment; DM/25 mGy, diabetic mice with LDR at 25 mGy; DM/50 mGy, diabetic mice with LDR at 50 mGy; DM/75 mGy, diabetic mice with LDR at 75 mGy.