1985 Volume 14 Issue 2 Pages 102-111
Decrease of serum triglyceride concentration and reciprocal increase of free fatty acid were observed at 30 minutes after intravenous administration of 300mg dextran sulfate in 5 healthy subjects, while serum total cholesterol and phospholipids were not affected. HDL cholesterol level was tended to increase, which was due to the increase of HDL2 cholesterol. HDL3 Cholesterol was not influenced essentially.
Serum VLDL concentration was markedly reduced by dextran sulfate. Although IDL and HDL were elevated, LDL level was unaffected. Above all, IDL triglyceride and HDL lipids incresed concomitantly.
Serum apo A-I, A-II, B, C-II, C-III and E protein concentrations were almost identical when compared with the pretreatment levels. However, apo B, C-II, C-III and E protein concentrations in VLDL fraction decreased remarkably following by the reduction of VLDL concentration. Since the changes of apo C-II and C-III concentration were noticeably, the percentages of these apoproteins in VLDL apoproteins became lower than those in the pretreatment. By contrast, apo C-II, C-III and E proteins increased in HDL fraction. The increases of apo C-II and C-III proteins were more pronaunced than that of apo E. Therefore, those apoproteins are considered to be transferred shift from VLDL to HDL by the lipolysis induced by dextran.
As for serum phospholipid fractions, the percentage of serum lysophosphatidyl choline increased, meanwhile the phosphatidyl choline/lysophosphatidyl choline ratio in serum and the percentage of phosphatidyl ethanolamine in VLDL decreased after the dextran sulfate injection. It suggests that dextran does not only stimulate lipoprotein lipase but also phospholipase activity at the same time as heparin.
