織田 直久

Using three month-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats as a NIDDM model and Long-Evans Tokushima Otsuka (LETO) rats as the control, we examined the effect of ACEI on the onset of diabetes mellitus. Oral administration of captopril (ACEI) was started from the age of 13 to 32 weeks (A group) and from the age of 25 to 32 weeks (B group). Oral GTT (oGTT) was performed at 4-week intervals from 12 weeks to 32 weeks of the age in OLETF and LETO rats. Body weights did not change significantly in either the A or B groups, compared with that in the control group. In oGTT for OLETF rats at 28 and 32 weeks of age, blood glucose levels in the A group were lower at 120 min after glucose administration than those in the B and control groups. In LETO rats, there were no significant changes in blood glucose levels in oGTT in any group. GLUT4 protein concentrations in the skeletal muscle and adipocytes were not significantly changed in any group. These data suggest that ACEI improves the glucose intolerance in NIDDM model rats through some factor other than changes in GLUT4 concentrations.

Using three month-old Otsuka Long-Evans Tokushima Fatty (OLETF) rats as a NIDDM model and Long-Evans Tokushima Otsuka (LETO) rats as the control, we examined the effect of ACEI on the onset of diabetes mellitus. Oral administration of captopril (ACEI) was started from the age of 13 to 32 weeks (A group) and from the age of 25 to 32 weeks (B group). Oral GTT (oGTT) was performed at 4-week intervals from 12 weeks to 32 weeks of the age in OLETF and LETO rats. Body weights did not change significantly in either the A or B groups, compared with that in the control group. In oGTT for OLETF rats at 28 and 32 weeks of age, blood glucose levels in the A group were lower at 120 min after glucose administration than those in the B and control groups. In LETO rats, there were no significant changes in blood glucose levels in oGTT in any group. GLUT4 protein concentrations in the skeletal muscle and adipocytes were not significantly changed in any group. These data suggest that ACEI improves the glucose intolerance in NIDDM model rats through some factor other than changes in GLUT4 concentrations.