Serum N-acetyl-beta-D-glucosaminidase profiles in type 1 diabetes secondary complications: Causes of changes and significance of determination
Authorized Users Only
Article (Published version)
MetadataShow full item record
The connection between changes in the activity of serum N-acetyl-beta-D-glucosaminidase (NAG, E.C.184.108.40.206) and iso-enzymes and degree of secondary complications was analyzed in four groups of type 1 diabetic patients (n=69): without complications (n=22); with retinopathy (n=16); with retinopathy and polyneuropathy (n= 13), and with retinopathy, neuropathy, and nephropathy (n=18). In all groups statistically significant higher (P lt 0.001) percent fraction of A form (83.84 +/- 6.09, 84.37 +/- 5.74, 81.76 +/- 6.02, 76.37 +/- 7.38%, resp.) and lower (P lt 0.001, P lt 0.01) fraction of B form (15.87 +/- 5.65, 15.66 +/- 5.74, 18.33 +/- 5.98, 23.63 +/- 7.38, resp.) in total NAG compared with the control (A = 69.38 +/- 4.79%, B = 30.61 +/- 4.78%) were found. The differences in A as well as B forms between diabetic groups were not statistically significant. Significant strong positive correlations between total NAG and glycemia (0.494-0.623), total NAG and A form (0.934-0.966), and A fo...rm and glycemia (0.512-0.638) were found in all groups. No correlation was found between the fractions of B and A forms, except in the fourth group. The A form of diabetic patients in the fourth group was more acidic compared with the control and other diabetic groups. It was concluded that the changes in serum NAG and isoenzymic profiles in diabetes are the consequence of its increased exocytose, especially of the A form, in hyperglycemia and posttranslational modifications of iso-enzymes. The total activity of serum NAG and iso-enzymic profiles cannot be used for monitoring the development and distinction of type 1 diabetes secondary complications.
Keywords:serum N-acetyl-beta-D-glucosaminidase / iso-enzymes A and B / type 1 diabetes / diabetic complications / retinopathy / neuropathy / nephropathy
Source:Journal of Clinical Laboratory Analysis, 2008, 22, 4, 307-313
- Wiley-Liss, Hoboken