Urinary PC-1 and N-acetyl-β-D-glucosaminidase activity in patients with type 2 diabetes treated with metformin, gliclazide or glibenclamide

Abstract

Background: Insulin resistance is a key feature of type 2 diabetes mellitus. Plasma cell differentiation antigen (PC-1) is an inhibitor of insulin receptor tyrosine kinase, and has been implicated in the pathogenesis of insulin resistance. Methods: Urinary excretion of PC-1 was determined in 45 newly detected, obese diabetic patients treated with metformin (16 patients), gliclazide (14 patients) or glibenclamide (15 patients). Urinary N-acetyl-β-D-glucosaminidase (NAGA), a lysosomal enzyme, was determined as a marker of tubular damage in diabetes. Results: Basal urinary PC-1 excretion in all three groups of diabetic patients was at the level of healthy controls. Treatment with oral hypoglycaemic drugs did not change significantly the group level or the number of patients in each group with increased PC-1 activity. Urinary excretion of NAGA in patients with type 2 diabetes was not statistically different from the control level. Metformin and gliclazide treatment did not change significantly the group levels of NAGA excretion. However, glibenclamide treatment produced an increased urinary NAGA excretion in the whole group, and in about twice as many patients as in the pre-treatment period.