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Clinical Chemistry, Vol 18, 1403-1406, Copyright © 1972 by the American Association for Clinical Chemistry
1 Istituto di Patologia Medica e Metodologica
Clinica, Università di Catania, 95123, Catania, Italy.
In each of 10 highly hyperglycemic decompensated
diabetics with ketoacidosis, we found a markedly
increased serum activity of two lysosomal hydrolases (N-acetyl-
-glucosaminidase and
-glucuronidase). This was also true to a lesser degree of
five diabetics with less severe decompensation
and without ketoacidosis. The activity of both
enzymes and the degree of hyperglycemia were
highly correlated. We think these enzymatic
changes result from a process of activation and
release of tissue lysosomal enzymes, probably
occurring in connection with the increased catabolism present in decompensated diabetes. Nonlysosomal (cytoplasmic or mitochondrial) enzymes
were less changed (aspartate and alanine aminotransferases) or normal (aldolase, lactate- and
malate dehydrogenase, and creatine kinase).
This indicates that tissue damage alone could not
account for the increased activity of the two
lysosomal hydrolases; it therefore seems primarily
to be due to involvement of lysosomes.
-glucosaminidase
-glucuronidase lysosomal enzymes atherosclerosis hepatic disease
Submitted on June 27, 1972
Accepted on August 29, 1972
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