Abstract
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. We measured urinary excretion of PC-1 (alkaline phosphodiesterase I), a potential factor of insulin resistance, and N-acetyl-beta-D-glucosaminidase (NAGA) in 62 type 1 diabetic patients with different damage to the kidney. 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. 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.
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