Studies of endotoxin-induced decrease in lipoprotein lipase activity.
A variety of invasive stimuli have been shown to induce hyperlipidemia due to impaired removal of triglyceride from the circulation. The mechanism by which endotoxin induces a deficiency in the activity of the key enzyme of triglyceride metabolism, lipoprotein lipase (LPL), has been studied. In C3H/HeN (endotoxin-sensitive) mice, LPL activity in adipose tissue was markedly suppressed 16 h after endotoxin administration. In contrast, the endotoxin-resistant C3H/HeJ mice were less sensitive to the suppressive effect of endotoxin on LPL activity. After endotoxin administration, a transferable factor had been detected in the blood of C3H/HeN mice 2 h after the injection of endotoxin that causes a suppression of adipose tissue LPL activity in C3H/HeJ mice as well as in C3H/HeN mice. Conditioned medium from the cultures of peritoneal exudate cells of C3H/HeN mice incubated in endotoxin also suppresses adipose tissue LPL in C3H/HeJ mice. These studies demonstrate that exudate cells produce a humoral factor in response to endotoxin, which suppresses adipose tissue LPL.
D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001202:Ascitic Fluid / Q000166:cytology; D004731:Endotoxins / Q000494:pharmacology*; D008071:Lipoprotein Lipase / Q000378:metabolism*; D051379:Mice; D008809:Mice, Inbred C3H; D014280:Triglycerides / Q000097:blood*
D004731:Endotoxins; D014280:Triglycerides; D008071:Lipoprotein Lipase