Glycosidase activities in the liver and kidney of hereditary diabetic mice.
Hereditary diabetic mice (NSY) were inbred from original streptozotocin diabetic ICR mice for 8-9 generations using hyperglycemia as an index. The normoglycemic ICR mice were used as controls for the NSY line. The nonfasting blood sugar level of the NSY mice was 305 +/- 14 mg/100ml, while their immunoreactive insulin level was 30 +/- 4 microU/ml (the values of the controls were 165 +/- 12 mg/100 ml and 79 +/- 14 microU/ml, respectively). beta-N-Acetylglucosaminidase [EC 3.2.1.29], beta-galactosidase [EC 3.2.1.23], alpha-glucosidase [EC 3.2.1.21], and alpha-mannosidase [EC 3.2.1.24] activities were determined in the 1,000 X g supernatant of the liver and the kidney of control and streptozotocin diabetic ICR mice and their NSY line. In the kidneys of the insulinopenic NSY mice, the beta-galactosidase and alpha-mannosidase activities were significantly decreased. No significant changes were found in liver enzyme activities. Insulin treatment increased the kidney beta-galactosidase activity signficantly. The insulinopenic state, which caused a decrease in the glycosidase activities in the kidney, could induce retarded breakdown of glycoprotein.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology* / Q000235:genetics; D006026:Glycoside Hydrolases / Q000378:metabolism*; D007668:Kidney / Q000201:enzymology* / Q000473:pathology; D008099:Liver / Q000201:enzymology* / Q000473:pathology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR
D006026:Glycoside Hydrolases