Hypertriglyceridemia, commonly observed in septic patients, may result from a decreased ability of tissues to remove plasma triacylglycerol due to depressed lipoprotein lipase activity. While endotoxin administration results in substantial decreases in muscle lipoprotein lipase activity, enzyme activity is increased in animals subjected to other forms of stress and trauma. The present study was initiated to compare changes in plasma triacylglycerol concentrations and tissue lipoprotein lipase activities in rats challenged with endotoxin or live Escherichia coli (iv or ip) or rats subjected to polymicrobial peritoneal sepsis. Sixteen hours post-treatment plasma triacylglycerol levels were increased 200 to 300% in endotoxin- and E. coli-treated rats but did not differ from control animals subjected to peritoneal sepsis. At the same time, endotoxin administration resulted in significant decreases in heart (71-80%), soleus muscle (52-74%), and adipose tissue (21-32%) lipoprotein lipase activity regardless of the route injected. Intravenous E. coli also lead to a decrease in the three tissues examined while ip administration of E. coli reduced muscle and adipose tissue but not heart lipoprotein lipase activity. In contrast to endotoxemic and E. coli bacteremic rats, polymicrobial peritonitis resulted in significant increases in heart (46-89%) and skeletal muscle (18-39%) lipoprotein lipase activity. Thus, hypertriglyceridemia is not necessarily a consequence of sepsis but occurred in endotoxemic and bacteremic states when muscle and adipose tissue lipoprotein lipase activities were reduced. These findings support the postulate that sepsis-induced hypertriglyceridemia is likely to be associated with a decreased ability of lipoprotein lipase-containing tissues to clear circulating triacylglycerol.
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