Lipoprotein receptor activity of peritoneal macrophages from insulin-deficient mice.

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.