Effect of Streptozotocin-Induced Hyperglycemia on Lipid Profiles, Formation of Advanced Glycation Endproducts in Lesions, and Extent of Atherosclerosis in LDL Receptor-Deficient Mice
Autor: | Florencia Casanada, Shiva Merat, Mary Sutphin, Peter D. Reaven, Wulf Palinski |
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Rok vydání: | 1997 |
Předmět: |
Glycation End Products
Advanced Male Very low-density lipoprotein medicine.medical_specialty Arteriosclerosis autoantibodies medicine.medical_treatment Clinical Sciences Glycation End Products Peptidyl-Dipeptidase A Cardiorespiratory Medicine and Haematology Streptozocin LDL Mice chemistry.chemical_compound Glycation Diabetes mellitus Internal medicine Receptors Animals Medicine arteriosclerosis diabetes business.industry Cholesterol Insulin lipid peroxidation Streptozotocin medicine.disease Lipids Endocrinology Receptors LDL Cardiovascular System & Hematology chemistry Hyperglycemia LDL receptor Advanced LDL oxidation Cardiology and Cardiovascular Medicine business advanced glycation endproducts medicine.drug |
Zdroj: | Arteriosclerosis, thrombosis, and vascular biology, vol 17, iss 10 |
ISSN: | 1524-4636 1079-5642 |
Popis: | Abstract Investigations into the mechanisms by which diabetes accelerates atherosclerosis have been hampered by the lack of suitable animal models. We hypothesized that streptozotocin-treated LDL receptor-deficient mice would be a good model of diabetic atherosclerosis because streptozotocin causes diabetes in the parent C57BL/6 strain and because in these mice diet-induced hypercholesterolemia leads to the formation of advanced atherosclerotic lesions throughout the aorta. Diabetes was induced in 18 mice by intraperitoneal injection of streptozotocin. Low-dose insulin was given subcutaneously to prevent excessive mortality and extreme elevations in triglyceride levels. The control group was subjected to sham injections. Both groups were fed a diet containing .075% cholesterol for six months. Average blood glucose was higher in the diabetic group than in the control group (257±67 mg/dL versus 111±7 mg/dL, P −/− mice. |
Databáze: | OpenAIRE |
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