Salmonella abortus equi endotoxin does not affect leptin plasma levels in healthy humans.

Figure 1. Host responses to intravenous injection in 5 healthy subjects of 0.4 ng/kg body weight (Ⅺ) or 0.8 ng/kg body weight (Ⅵ) S. abortus equi endotoxin. For all variables, mean differences between endotoxin and placebo conditions at every time point are depicted. of mean. For description of results and for statistics, see Bars ϭ SE text. To the Editor—We read with interest the recent paper of Born-stein et al. [1], who report that 4 ng/kg body weight Escherichia coli endotoxin injected intravenously into healthy volunteers fails to increase circulating leptin levels, despite a clear-cut activation of the hypothalmo-pituitary-adrenal system and an increase in rectal temperature. This finding is surprising, because endotoxin has been shown to stimulate leptin production in animals [2] and because the administration of pivotal mediators of endotoxin's effects on host defense, such as tumor necrosis factor-a (TNF-a) [3] and glucocorticoids [4], has been shown to increase leptin levels in humans. We report here on the effects of another endotoxin preparation on rectal temperature, and on the plasma levels of interleukin-6 (IL-6), TNF-a, and cor-tisol in healthy volunteers. The study comprised 10 male subjects (age: years). 26 ‫ע‬ 4 Five subjects received 0.4 ng/kg body weight and 5 received 0.8 ng/kg body weight Salmonella abortus equi endotoxin (for details about the endotoxin preparation see [5]) intravenously in a single-blind placebo-controlled design. On two experimental occasions separated by 2 weeks, they fasted, starting at 7 p.m. Endotoxin or 0.9% saline solution was injected at 11 p.m., when temperature and cortisol responses are much more pronounced than in the morning [6]. After the injection, the subjects were kept awake throughout the experiment. They participated in a larger study of the interactions between host responses to en-dotoxin and sleep-wake behavior (the respective results will be presented elsewhere). Rectal temperature was monitored continuously, and blood samples were taken through an intravenous catheter. Plasma was frozen to Ϫ20ЊC. IL-6 and TNF-a levels were determined by ELISAs (Medgenix Diagnostics, Brussels); RIAs were used to measure cortisol (ICN Biomedicals, Carson, CA) and leptin (DRG Instruments, Marburg, Germany) levels. The effects of endotoxin (expressed as the difference between values obtained