Loading…
Hydrolase Activities in the Rat Aorta: I. Effects of Diabetes Mellitus and Insulin Treatment
SUMMARY Vascular disease in diabetics could arise in part from altered vessel wall catebolism. Specific activities of hydrolases in aortic smooth muscle cells from rats with streptozotocin-induced diabetes were measured. Enzymes includedneutral α-glucosidase, α-mannosidase, and lysosomal /V-acetyl β...
Saved in:
Published in: | Circulation research 1978-06, Vol.42 (6), p.821-831 |
---|---|
Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | SUMMARY Vascular disease in diabetics could arise in part from altered vessel wall catebolism. Specific activities of hydrolases in aortic smooth muscle cells from rats with streptozotocin-induced diabetes were measured. Enzymes includedneutral α-glucosidase, α-mannosidase, and lysosomal /V-acetyl β-glucosaminidase, β-galactosidase, cathepsin C, acid α-glucosidase, and acid cholesteryl esterase. After 4,8, and 11 weeks of diabetes, activities of all enzymes studied were decreased significantly in diabetic vessels, decreases ranging from 15% for cathepsin C to 62% for amannosidase. After 3 weeks of diabetes, insulin treatment for 1 week restored enzyme levels to normal. After 7 weeks of diabetes, 1 week of insulin treatment did not restore enzyme levels fully to normal (acid cholesteryl esterase was unchanged); 4 weeks of insulin did. Acid phosphatase and JV-acetyl β-glucosaminidase activities were reduced markedly in histochemical studies of diabetic aortas at all time periods and were restored by insulin treatment. AUoxan-induced diabetes gave results similar to those with streptozotocin. Significant decreases of aortic hydrolase activities, including those of lysosomes, occur in experimental diabetes mellitus and could contribute to accumulation of substrates in vascular smooth muscle cells. |
---|---|
ISSN: | 0009-7330 1524-4571 |
DOI: | 10.1161/01.res.42.6.821 |