Endotoxin inhibits catabolism of low density lipoproteins in vivo: an experimental study in the rat.
Hyperlipidaemia frequently accompanies infectious diseases and may be due to an increase in lipoprotein production or a decrease of lipoprotein clearance. The administration of endotoxin has been used to mimic infection and previous studies have demonstrated that endotoxin induces an increase in low density lipoprotein (LDL) levels. In the present study in rats, the dose of endotoxin (055:B5, 50 micrograms 100 g body weight-1) induced hyperlipidaemia without shock and death. The clearance of 125I-LDL was measured after simultaneous injection of 100 micrograms LDL protein with endotoxin or without endotoxin (control). Endotoxin significantly inhibited the clearance of 125I-LDL from blood at all time intervals between 1 and 24 h. The total 125I and trichloroacetic acid-(TCA) precipitable 125I in the liver was higher in endotoxin-treated animals than in controls after 0.5, 4 and 24 h. An increased tissue radioactivity was also seen in several other tissues at various time intervals in the endotoxin treated group. The increase in plasma triglyceride induced by endotoxin reached a maximum after 8 h. Endotoxin thus causes a rapid inhibition of both the LDL disappearance from blood and of the LDL degradation after the uptake by the liver. This effect precedes the increase in triglyceride levels. The inhibition of the LDL catabolism may contribute to the rise in LDL levels in endotoxin induced hyperlipidaemia.
Xu
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Department of Cell Biology 1, University Hospital of Lund, Sweden.
Nilsson
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A
D000818:Animals; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli; D007457:Iodine Radioisotopes; D007700:Kinetics; D008077:Lipoproteins, LDL / Q000097:blood / Q000378:metabolism*; D008297:Male; D008657:Metabolic Clearance Rate; D051381:Rats; D017207:Rats, Sprague-Dawley; D014280:Triglycerides / Q000097:blood
D004731:Endotoxins; D007457:Iodine Radioisotopes; D008077:Lipoproteins, LDL; D014280:Triglycerides