OBJECTIVES: In this study, we investigated clinically, pathologically, and immunohistochemically the effect of insufficient short-acting insulin treatment on streptozotocin (STZ)-induced diabetes mellitus in rats. METHODS: Three groups composed of 10 rats each were studied as follows: (1) a group that received only STZ (50 mg/kg) (STZ group); (2) a group that received 50 mg/kg STZ and, after 12 hours, 8 IU of short-acting insulin treatment (STZ + INS group), repeated every night for 5 days; and (3) a control group. Ketonuria and blood glucose levels were examined every day. Blood was obtained from 2 rats from each group, and necropsy was performed every day during the 5-day period. RESULTS: Hyperglycemia was observed in the STZ and STZ + INS groups 24 hours after, but levels were higher in the STS + INS group than those in the STZ-only group. Histopathology was similar in the STZ and STZ + INS groups, and degeneration was observed in both groups, but immunohistochemistry revealed a more severe reduction in insulin-secreting cells in the STZ + INS group than that in the STZ group. There were no hyperglycemia and histopathological or immunochemical alteration in the control group. CONCLUSIONS: This study showed that insufficient short-acting insulin treatment can increase the diabetogenic effect of STZ in rats.
OBJECTIVES: In this study, we investigated clinically, pathologically, and immunohistochemically the effect of insufficient short-acting insulin treatment on streptozotocin (STZ)-induced diabetes mellitus in rats. METHODS: Three groups composed of 10 rats each were studied as follows: (1) a group that received only STZ (50 mg/kg) (STZ group); (2) a group that received 50 mg/kg STZ and, after 12 hours, 8 IU of short-acting insulin treatment (STZ + INS group), repeated every night for 5 days; and (3) a control group. Ketonuria and blood glucose levels were examined every day. Blood was obtained from 2 rats from each group, and necropsy was performed every day during the 5-day period. RESULTS:Hyperglycemia was observed in the STZ and STZ + INS groups 24 hours after, but levels were higher in the STS + INS group than those in the STZ-only group. Histopathology was similar in the STZ and STZ + INS groups, and degeneration was observed in both groups, but immunohistochemistry revealed a more severe reduction in insulin-secreting cells in the STZ + INS group than that in the STZ group. There were no hyperglycemia and histopathological or immunochemical alteration in the control group. CONCLUSIONS: This study showed that insufficient short-acting insulin treatment can increase the diabetogenic effect of STZ in rats.