Butera Peter C, Briffa Christopher F, Whitaker Emmett E
Department of Psychology, Niagara University, P.O. Box 2208, Niagara, NY 14109-2208, USA.
Physiol Behav. 2004 Oct 15;82(5):777-83. doi: 10.1016/j.physbeh.2004.06.018.
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 CCK(A) 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 microg) 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 microg/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.
感染过程中释放的促炎细胞因子会引发众多行为和代谢变化。感染时伴随出现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）是进食期间释放的一种神经肽，会减少食物摄入量，先前的研究表明CCK介导了IL-1的厌食作用。雌激素对食物摄入量的影响也被认为与CCK有关，因为在完整大鼠和去卵巢大鼠中，雌二醇都会增强CCK的饱腹感作用。雌二醇还能调节IL-1的许多行为和生理效应。本实验研究了CCK（A）受体拮抗剂地伐西匹阻断IL-1和雌二醇对雌性大鼠食物摄入量影响的能力。成年动物接受去卵巢手术，术后3周每天皮下注射两次苯甲酸雌二醇（EB；5.0微克）或油性赋形剂。治疗开始3天后，在腹腔注射IL-1β（4.0微克/千克）或在光照熄灭前1小时注射生理盐水前30分钟，给动物注射地伐西匹或其赋形剂进行预处理。在自发进食2小时后测量食物和水的摄入量。结果表明，尽管地伐西匹阻断了雌二醇对食物摄入量的影响，但它未能逆转IL-1β的厌食作用。这些数据不支持CCK在IL-1诱导的厌食中起作用，并表明细胞因子可能直接作用于参与食物摄入控制的神经系统。
