McCarthy D O, Kluger M J, Vander A J
Physiol Behav. 1986;36(4):745-9. doi: 10.1016/0031-9384(86)90363-x.
We have previously shown that interleukin-1 (IL-1), a polypeptide known to mediate many aspects of the acute phase response to infection, suppresses food intake when injected intraperitoneally into fasted rats. IL-1 acts at the level of the hypothalamus to induce fever. In view of the large number of peptides that have been shown to alter food intake as well as body temperature when injected intracerebroventricularly (ICV), we hypothesized that the receptor site for the anorexigenic activity of IL-1 would be located in a central nervous site bathed by the cerebrospinal fluid. In the present study, ICV injection of IL-1 or E. coli endotoxin (a stimulus for the synthesis of IL-1), significantly elevated body temperature, but did not affect food intake of fasted rats. We conclude that receptors mediating the anorexigenic actions of IL-1 or endotoxin are not located at a central nervous site bathed by the cerebrospinal fluid. Furthermore, fever per se is not responsible for the reduction in food intake seen following peripheral injection of IL-1 or endotoxin.
我们之前已经表明,白细胞介素-1(IL-1)是一种已知可介导感染急性期反应诸多方面的多肽,当腹腔注射到禁食大鼠体内时,它会抑制食物摄入。IL-1在下丘脑水平起作用以诱导发热。鉴于大量多肽经脑室注射(ICV)后已被证明会改变食物摄入以及体温,我们推测IL-1的厌食活性受体位点将位于被脑脊液浸润的中枢神经部位。在本研究中,ICV注射IL-1或大肠杆菌内毒素(一种IL-1合成的刺激物)显著升高了体温,但不影响禁食大鼠的食物摄入。我们得出结论,介导IL-1或内毒素厌食作用的受体并不位于被脑脊液浸润的中枢神经部位。此外,发热本身并非外周注射IL-1或内毒素后食物摄入减少的原因。