Changes in plasma hydrolase activities in hereditary and streptozotocin-induced diabetes

Abstract

Reports of elevated plasma levels of acid hydrolases in diabetic patients prompted us to investigate these enzymes in genetically diabetic (db/db) mice and in streptozotocintreated rats and mice. The homozygous (db/db) mice showed decreased, rather than increased, levels of plasma hydrolases as compared to their heterozygous (db/+) nondiabetic controls. Similarly, mice (Swiss and db/+) with streptozotocin-induced diabetes showed lowered plasma hydrolase activities. On the other hand, drug-induced diabetes in rats was accompanied by increased hydrolase levels, the increase being reversed by insulin treatment. In investigating the underlying mechanism of the changes observed in rats, leukocytes and blood platelets were ruled out as sources of the additional plasma lysosomal enzymes, and evidence was obtained suggesting that the diabetic animal was normal in regard to the ability to remove lysosomal glycosidase from blood. However, perfusion of diabetic liver resulted in release of more acid hydrolase activity than did perfusion of normal liver, and perfusion with glucagon stimulated enzyme release. These results suggest that liver is a possible source of the added enzyme found in streptozotocin-treated rat plasma.