ABSTRACT
The mechanism of the hypoglycaemic action of sulfonylurea agents remains controversial, in spite of the fact that they have been widely used in the clinical management of patients with NIDDM. in this study, we used insulin clearance and euglycaemic clamp technique in order to investigate the extapancreatic effect of glipizide. Forty-five non insulin dependent diabetes (NIDDM) patients were included in insulin clearance study (F:M 25:20, mean age 43.1±4.6, mean duration of diabetes: 5.1±1.2 years). Euglycaemic clamp technique was performed in 15 of these patients (F:M 8:7, mean age 42.7±4.2, mean duration of diabetes 4.9±1.9 years). Pre-treatment mean insulin clearance value of 21.37 was reduced to 8.54 (p<0.0001). Pre-treatment m/l value was 1.51 mg/µU and 3 months after glipizide treatment this value was increased to 1.78 mg/µU (p<0.05). in conclusion, it may be argued for the role of glipizide in lowering peripheric insulin resistance; in other words glipizide may increase insulin binding to insulin receptors.
The mechanism of the hypoglycaemic action of sulfonylurea agents remains controversial, in spite of the fact that they have been widely used in the clinical management of patients with NIDDM. in this study, we used insulin clearance and euglycaemic clamp technique in order to investigate the extapancreatic effect of glipizide. Forty-five non insulin dependent diabetes (NIDDM) patients were included in insulin clearance study (F:M 25:20, mean age 43.1±4.6, mean duration of diabetes: 5.1±1.2 years). Euglycaemic clamp technique was performed in 15 of these patients (F:M 8:7, mean age 42.7±4.2, mean duration of diabetes 4.9±1.9 years). Pre-treatment mean insulin clearance value of 21.37 was reduced to 8.54 (p<0.0001). Pre-treatment m/l value was 1.51 mg/µU and 3 months after glipizide treatment this value was increased to 1.78 mg/µU (p<0.05). in conclusion, it may be argued for the role of glipizide in lowering peripheric insulin resistance; in other words glipizide may increase insulin binding to insulin receptors.