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.
