Watson P J, Leitner C
Psychology Department, University of Tennessee, Chattanooga 37403.
Physiol Behav. 1988;43(6):697-704. doi: 10.1016/0031-9384(88)90366-6.
In previous research, 750 mg/kg 2DG yielded a number of effects suggesting a postdrug nausea; and the present experiments revealed that the illness-inducing agent LiCl similarly produced taste aversion learning at 7.5 mg/kg, inhibited drinking in water-deprived animals at 30 mg/kg, depressed feeding in hungry rats at 60 mg/kg, and evoked food intake and pica at 120 mg/kg. The appearance of eating and pica at the same dosage suggested that rats may eat food as well as a nonnutritive substance as a species-specific reaction to illness and that postdrug feeding, including that observed after 2DG, is an insufficient condition for concluding that a treatment produces no internal distress. A liquid diet that reportedly ameliorates the glucoprivic feeding deficits produced by lateral hypothalamic and zona incerta lesions theoretically could produce its effects if lesions made rats more reactive to 2DG-induced malaise and if this diet were more palatable to animals experiencing internal distress. However, this liquid diet failed to facilitate food intake after LiCl, nor did it reduce the inhibited eating produced by LiCl in food-deprived subjects. Liquid diet effects in lesioned animals, therefore, may not be explained by factors related to a 2DG-induced malaise.
在先前的研究中,750毫克/千克的2-脱氧-D-葡萄糖(2DG)产生了一系列表明用药后恶心的效应;而目前的实验表明,致病情剂氯化锂(LiCl)在7.5毫克/千克时同样能产生味觉厌恶学习,在30毫克/千克时抑制缺水动物的饮水,在60毫克/千克时抑制饥饿大鼠的进食,并在120毫克/千克时引发食物摄入和异食癖。相同剂量下出现进食和异食癖表明,大鼠可能会将食物以及非营养物质作为对疾病的一种物种特异性反应来食用,并且用药后的进食,包括2DG后观察到的进食,不足以得出一种治疗不会产生内部不适的结论。据报道,一种液体饮食可改善由下丘脑外侧和未定带损伤引起的糖缺乏性进食缺陷,理论上,如果损伤使大鼠对2DG诱导的不适更敏感,并且这种饮食对经历内部不适的动物更可口,那么它可能会产生效果。然而,这种液体饮食未能促进LiCl后的食物摄入,也没有减少LiCl在食物缺乏的实验对象中引起的进食抑制。因此,液体饮食对损伤动物的影响可能无法用与2DG诱导的不适相关的因素来解释。