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.
Cheng
G
G
Department of Biochemistry, Tongji Medical University, Wuhan.
Wang
H X
HX
Zhang
J M
JM
Zong
Y X
YX
Feng
Z C
ZC
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D008079:Lipoproteins, VLDL / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D051379:Mice; D010529:Peritoneal Cavity / Q000166:cytology; D011973:Receptors, LDL / Q000378:metabolism*
D008079:Lipoproteins, VLDL; D011973:Receptors, LDL; C036053:VLDL receptor