title: Metabolic disorders of serum lipoproteins in endotoxin-poisoned mice: the role of high density lipoprotein (HDL) and triglyceride-rich lipoproteins.
abstract: A study was performed to clarify the role of serum lipoproteins, especially high density lipoprotein (HDL) and triglyceride-rich lipoproteins in endotoxemic or endotoxin-poisoned animals. The level of HDL-cholesterol decreased markedly in mouse serum 18-24 hr postintoxication, while the amount of low density lipoprotein (LDL)-cholesterol in the sera of poisoned mice was about 175% of that of the controls. Serum lecithin-cholesterol acyltransferase activity in the poisoned mice decreased slightly for 3-6 hr after endotoxin injection, but became markedly increased at 18-24 hr as compared with that in the controls. The amount of serum very low density lipoprotein (VLDL) showed a marked increase in the poisoned mice 8-24 hr postintoxication. The HDL fraction in the electrophoretic patterns of serum was reduced according to the dose of endotoxin 18 hr postintoxication. The HDL fraction in mice injected with lead acetate plus endotoxin was markedly lower than that in the poisoned mice. When streptozotocin-diabetic mice were injected with endotoxin, the HDL fraction was higher than that in the endotoxin-poisoned mice. In endotoxin-poisoned mice a correlation was observed between the lipid peroxide and LDL levels in the serum. In disk electrophoretic patterns, the HDL fraction in mice given vitamin E-supplemented diet showed a higher level than that in mice given a normal diet. Lipoprotein lipase (LPL) activity in poisoned mice significantly decreased to 59% of the control value 18 hr postintoxication, but hepatic triglyceride lipase activity was only slightly increased in endotoxin-poisoned mice. In analysis of HDL apoprotein peptide in serum lipoprotein, the apo C-II peptide level was clearly lower in mouse serum 18 hr postintoxication than that in the controls. These results suggest that the decrease in LPL activity in endotoxin-poisoned mice may be closely related to a decrease in the apo C-II peptide level, and also that it plays an important part in HDL and triglyceride-rich lipoprotein metabolism in the poisoned mice.
mesh_terms: D000818:Animals; D053304:Apolipoprotein C-II; D001053:Apolipoproteins / Q000097:blood; D001056:Apolipoproteins C; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism; D004731:Endotoxins / Q000506:poisoning*; D007854:Lead / Q000494:pharmacology; D008049:Lipase / Q000378:metabolism; D008054:Lipid Peroxides / Q000378:metabolism; D008074:Lipoproteins / Q000097:blood*; D008075:Lipoproteins, HDL / Q000097:blood*; D008077:Lipoproteins, LDL / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D008099:Liver / Q000378:metabolism; D008297:Male; D051379:Mice; D009942:Organometallic Compounds; D007862:Phosphatidylcholine-Sterol O-Acyltransferase / Q000097:blood; D013311:Streptozocin / Q000494:pharmacology; D014280:Triglycerides / Q000097:blood*; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D053304:Apolipoprotein C-II; D001053:Apolipoproteins; D001056:Apolipoproteins C; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D004731:Endotoxins; D008054:Lipid Peroxides; D008074:Lipoproteins; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL; D009942:Organometallic Compounds; D014280:Triglycerides; C030087:lipoprotein triglyceride; D014810:Vitamin E; D007854:Lead; D013311:Streptozocin; D002784:Cholesterol; D007862:Phosphatidylcholine-Sterol O-Acyltransferase; D008049:Lipase; C008261:lead acetate