SEQUENTIAL ALTERATIONS IN TISSUE LIPOPROTEIN-LIPASE, TRIGLYCERIDE SECRETION RATES, AND SERUM TUMOR-NECROSIS-FACTOR-ALPHA DURING ESCHERICHIA-COLI BACTEREMIC SEPSIS IN RELATION TO THE DEVELOPMENT OF HYPERTRIGLYCERIDEMIA

The time sequence and the mechanisms leading to the development of the hypertriglyceridemia of bacteremic sepsis are not fully understood, T his study was conducted to determine the mechanisms leading to the ear ly rise in serum triglycerides (TG). Bacteremic sepsis was induced in fasted and parenterally fed rats by intravenous infusion of live Esche richia coli colonies over a 1 h period every 24 h up to 98 h. Body tem perature was elevated from 12 to 48 h after E. coli infusion in fasted rats and from 24 to 72 h after E. coli infusion in fed rats, The init ial rise in serum TG was observed at 3 h after E. coli infusion; in fa sted rats this elevation was maintained over 72 h, In the parenterally fed rats, hypertriglyceridemia was evident only at the 3 h time point , Serum concentrations of tumor necrosis factor alpha (TNF-alpha) were elevated significantly at 60 min after initiating the E. coli infusio n, peaked at 90 min, and declined by 120 min. Immunization with neutra lizing goat anti-TNF-alpha IgG did not block the initial increase in s erum TG induced by E. coli. This early rise in TG in fasted E. coli-tr eated rats was accompanied by a 33% increase in TG secretion in compar ison with control rats. TG secretion declined by 27% at 9 h and remain ed depressed at 12 and 24 h in comparison with time-matched control ra ts. By 24 h lipid accumulation was evident in the livers of the fasted and fed E. coli-treated rats. Most of the fasted E. coli-treated rats died by 72 h. Parenteral feeding extended survival of E. coli-treated rats until 120 h. These findings along with the observation that two mechanisms are involved in maintaining the elevation of serum TG durin g E. coli sepsis suggests that the hypertriglyceridemia may be importa nt in host survival.