Background: Insulin resistance characterizes type 1 diabetes mellitus
with nephropathy. The molecular mechanisms of insulin resistance are not completely
understood. Recently some advances have been made in identification of transmembrane
glycoprotein PC-1 as a potential factor of insulin resistance.
Methods: We measured urinary excretion of PC-1 (alkaline
phosphodiesterase I), a potential factor of insulin resistance, and
N-acetyl-β-D-glucosaminidase (NAGA) in 62 type 1 diabetic patients with different
damage to the kidney.
Results: In newly detected type 1 diabetes patients, before insulin
therapy, urine PC-1 excretion was significantly increased (P<0·05) over the
control level. However, in patients after 12·4 years of therapy, urinary PC-1 was
significantly decreased (P<0·05). Decreased urine PC-1 activity (P<0·05) was
found also in type 1 diabetes patients with microalbuminuria and manifest
nephropathy, including those with renal failure. Urinary NAGA excretion was found to
be significantly increased (P=0·001) in all but the group of type 1 diabetes patients
without nephropathy.
Conclusion: This study of urinary PC-1 in patients with type 1 diabetes
shows increased excretion in newly detected patients with poor glycaemic control, but
decreased excretion in patients with micro-/macroalbuminuria as well as in those
without apparent kidney damage. In patients with primary glomerulonephritis, urinary
excretion of PC-1 was significantly decreased and that of NAGA significantly
increased compared with the excretion in healthy controls.
