Lipoprotein receptor activity of peritoneal macrophages from insulin-deficient mice
| Autor: | J Zhang, Zong Yx, Zong-chen Feng, Cheng G, H Wang |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Male
medicine.medical_specialty Very low-density lipoprotein Arteriosclerosis medicine.medical_treatment Lipoproteins VLDL digestive system Diabetes Mellitus Experimental Pathogenesis Mice Peritoneal cavity Management of Technology and Innovation Internal medicine Diabetes mellitus polycyclic compounds medicine Animals Receptor Peritoneal Cavity Chemistry Macrophages Insulin nutritional and metabolic diseases medicine.disease Streptozotocin medicine.anatomical_structure Endocrinology Receptors LDL Biochemistry lipids (amino acids peptides and proteins) medicine.drug |
| Zdroj: | Journal of Tongji Medical University. 11:193-197 |
| ISSN: | 0257-716X |
| DOI: | 10.1007/bf02888149 |
| Popis: | Binding, uptake and degradation of 125I-labeled normal very low density lipoprotein (125I-n-VLDL) from normal swine plasma and 125I-labeled beta-migrating VLDL (125I-beta-VLDL) from hypercholesterolemic rabbit plasma by peritoneal macrophages of mice rendered insulin-deficient by streptozotocin (250 mg/kg) were studied. It was found that the amount of binding, uptake and degradation of 125I-n-VLDL by macrophages from the diabetic mice was 2-fold or 2.5-fold higher than by macrophages from normal mice, resulting from an increase in the binding capacity of VLDL receptors on the macrophages from the insulin-deficient rodents. In contrast, the binding, uptake and degradation of 125I-beta-VLDL by macrophages from diabetic mice were reduced to only about 45% of normal levels because of a decrease in the number and affinity of the receptors for beta-VLDL. These experimental results indicate that n-VLDL is more important than beta-VLDL in the pathogenesis of atherosclerosis in insulin-dependent diabetes. |
| Databáze: | OpenAIRE |
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