Devazepide fails to reverse the inhibitory effect of interleukin-1β on food intake in female rats
Devazepide fails to reverse the inhibitory effect of interleukin-1β on food intake in female rats
复制标题
DOI：
10.1016/j.physbeh.2004.06.018
复制
发表时间：
2004-10-15
影响因子：
2.9
通讯作者：
Whitaker, EE
中科院分区：
文献类型：
--
作者：
Butera, PC;Briffa, CF;Whitaker, EE
感染过程中释放的促炎细胞因子引起许多行为和代谢变化。感染引起的食物摄入量减少部分是由白细胞介素-1 (IL-1) 介导的。胆囊收缩素 (CCK) 是一种在进餐时释放的神经肽，可减少食物摄入量，之前的研究表明 CCK 介导 IL-1 的食欲减退作用。雌激素对食物摄入的影响也被认为与 CCK 相关，因为在完整大鼠和卵巢切除大鼠中，雌二醇都会增加 CCK 的饱腹感作用。雌二醇还调节 IL-1 的许多行为和生理效应。本实验检查了 CCKA 受体拮抗剂地维西派阻断 IL-1 和雌二醇对雌性大鼠食物摄入的影响的能力。成年动物被切除卵巢，并在手术后3周每天皮下注射雌二醇苯甲酸酯（EB；5.0杯）或油媒介物两次。治疗开始三天后，在腹膜内注射IL-1β（4.0杯/千克）或在光抵消前1小时给予盐水之前30分钟，用地维西必或其载体对动物进行预处理。自主进食2小时后测量食物和水的摄入量。结果表明，尽管地维西派阻断了雌二醇对食物摄入的影响，但地维西派未能逆转IL-1β的厌食作用。这些数据不支持 CCK 在 IL-1 诱导的厌食症中的作用，并表明细胞因子可能直接作用于参与控制食物摄入的神经系统。 (C) 2004 Elsevier Inc. 保留所有权利。
Proinflammatory cytokines released during the course of infection elicit numerous behavioral and metabolic changes. The decrease in food intake that accompanies infection is mediated in part by interleukin-1 (IL-1). Cholecystokinin (CCK) is a neuropeptide released during a meal, decreases food intake, and previous research suggests that CCK mediates the anorectic action of IL-1. The effects of estrogen on food intake are also thought to involve CCK, as the satiety action of CCK is increased by estradiol in both intact and ovariectomized rats. Estradiol also modulates many of the behavioral and physiological effects of IL-1. The present experiment examined the ability of the CCKA receptor antagonist devazepide to block the effects of IL-1 and estradiol on food intake in female rats. Adult animals were ovariectomized and given two daily subcutaneous injections of estradiol benzoate (EB; 5.0 mug) or the oil vehicle 3 weeks after surgery. Three days after treatment onset, animals were pretreated with devazepide or its vehicle 30 min prior to intraperitoneal injections of IL-1beta (4.0 mug/kg) or saline given 1 h before light offset. Food and water intake was measured following 2 h of spontaneous feeding. The results indicate that devazepide failed to reverse the anorectic action of IL-1beta, although the effects of estradiol on food intake were blocked by devazepide. These data do not support a role for CCK in IL-1-induced anorexia, and suggest that cytokines may act directly on neural systems involved in the control of food intake. (C) 2004 Elsevier Inc. All rights reserved.