Abstract
A variety of invasive stimuli induce hyperlipidemia due to impaired removal of triglyceride from the circulation. The mechanism by which endotoxin [from Escherichia coli] induces a deficiency in the activity of the key enzyme of triglyceride metabolism, lipoprotein lipase (LPL), was studied. In C3H/HeN (endotoxin-sensitive) mice, LPL activity in adipose tissue was markedly suppressed 16 h after endotoxin administration. Entotoxin-resistant C3H/HeJ mice were less sensitive to the suppressive effect of endotoxin of LPL activity. A transferable factor, detected in the blood of C3H/HeN mice 2 h after endotoxin injection, causes a suppression of adipose tissue LPL activity in C3H/HeJ mice and 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. Evidently, in response to endotoxin, exudate cells produce a humoral factor which suppresses adipose tissue LPL.