Fushimi H, Tarui S
Clin Chim Acta. 1976 Aug 16;71(1):1-8. doi: 10.1016/0009-8981(76)90267-9.
In previous studies, beta-N-acetyglucosaminidase activities were found to be markedly decreased in streptozotocin diabetic rat kidney, while that of the liver, spleen and intestine remained unchanged. The decrease in total kidney enzyme activity was in parallel with a decrease in the enzyme activity of the main isozyme of beta-N-acetylglucosaminidase, of which little or none was contained in the other three tissues. The present paper reports that the retina, also sensitive to diabetic microangiopathy, showed a similar isozyme pattern to that of kidney, composed of mainly type II isoenzyme of beta-N-acetylglucosaminidase. Type II isoenzyme was not detectable in any of the other materials tested including human and rat erythrocytes, lymphocytes and platelets, and human buccal epithelia and saliva, except human tear. The physiologic significance of the human tear beta-N-acetylglucosaminidase is unknown, but this enzyme was found to contain a considerable amount of Type II isoenzyme, and the enzyme activities were decreased in poorly controlled diabetic patients. Patients with retinopathy also showed markedly lowered tear enzyme activity. The diabetic patients were followed up for several months with occasional ophthalmoscopic examination and determination of serum beta-N-acetylglucosaminidase activity. As a result, changes in the latter were found to be useful as an indicator of the development of microangiopathy.