Daun J M, McCarthy D O
School of Nursing, University of Wisconsin-Madison 53792.
Physiol Behav. 1993 Aug;54(2):237-41. doi: 10.1016/0031-9384(93)90105-o.
Anorexia is a common response to infection which is thought to be mediated, at least in part, by interleukin (IL-1), an immunoregulatory peptide secreted by activated monocytes. Cholecystokinin (CCK) is a neuropeptide that suppresses food intake and gastric emptying when injected into healthy animals. There is increasing evidence of bidirectional interactions between neuropeptides, immune cell function, and secretion of immunoregulatory cytokines. Therefore, the present study was undertaken to determine if administration of L364,718 (L364), a CCK receptor antagonist, might block the anorexigenic effects of recombinant human IL-1 alpha (IL-1 alpha) in rats. We report that injection of IL-1 alpha significantly increased plasma CCK 1 h after injection, and decreased food intake and emptying of gastric contents. Pretreatment with 1 mg/kg L364 partially blocked the decrease in food intake and gastric stasis induced by IL-1 alpha. We conclude CCK may mediate, at least in part, IL-1 alpha-induced anorexia.
厌食是对感染的一种常见反应，人们认为这至少部分是由白细胞介素（IL-1）介导的，IL-1是一种由活化单核细胞分泌的免疫调节肽。胆囊收缩素（CCK）是一种神经肽，当注射到健康动物体内时会抑制食物摄入和胃排空。越来越多的证据表明神经肽、免疫细胞功能和免疫调节细胞因子的分泌之间存在双向相互作用。因此，本研究旨在确定给予CCK受体拮抗剂L364,718（L364）是否可能阻断重组人IL-1α（IL-1α）对大鼠的致厌食作用。我们报告，注射IL-1α后1小时，血浆CCK显著增加，食物摄入量和胃内容物排空减少。用1mg/kg L364预处理可部分阻断IL-1α诱导的食物摄入量减少和胃淤滞。我们得出结论，CCK可能至少部分介导IL-1α诱导的厌食。
