Hammond P B, Minnema D J, Shulka R
Department of Environmental Health, University of Cincinnati, Ohio 45267-0056.
Toxicol Appl Pharmacol. 1990 Oct;106(1):80-7. doi: 10.1016/0041-008x(90)90108-7.
Lead (Pb) depresses growth in infants and young children. Our earlier studies using a weanling rat model of Pb exposure suggest that this Pb effect is due to depression of appetite. In the present study we examined whether this depression of appetite is consistent with a down-regulation of the appetite "set point" as described using dietary manipulations following either lesions of certain hypothalamic regions or 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure. Two types of dietary manipulations were employed: (a) consumatory response to hyperalimentation (force-feeding), and (b) consumatory and growth response during the catch-up period following food restriction. In the hyperalimentation experiments, food intake was determined (a) with and without force-feeding, and (b) without Pb and with Pb administered either orally or systemically. Pb exposure reduced food consumption compared to controls. Force-feeding of a liquid diet further reduced food consumption, but only to the level that maintained total caloric intake at, or close to, the level of Pb animals not force-fed. In the food-restriction experiments, weanling rats had their food intake restricted for 4 days and then were provided free access to food, at which time one subgroup of these animals was exposed to Pb. Catch-up of previously food-restricted animals, in terms of food consumption and growth, was the same in the first 2 days, regardless of whether Pb was administered. During the next 10 days, the food intake and growth of the non-Pb-exposed, food-restricted animals gradually converged on the previously free-fed, non-Pb-exposed animals, whereas the food-restricted. Pb-exposed animals converged on the growth-depressed, previously free-fed Pb-exposed animals. All these responses to dietary manipulations are consistent with a reduced set point for appetite rather than with a nonspecific effect of Pb, e.g., aversion to food or general malaise.
铅(Pb)会抑制婴幼儿的生长。我们早期使用幼鼠铅暴露模型的研究表明,这种铅效应是由于食欲下降所致。在本研究中,我们探讨了这种食欲下降是否与食欲“设定点”的下调一致,这一概念是通过对特定下丘脑区域损伤或2,3,7,8 - 四氯二苯并 - p - 二恶英暴露后进行饮食操作来描述的。我们采用了两种饮食操作方式:(a)对过度喂养(强制喂食)的消耗性反应,以及(b)食物限制后的追赶期内的消耗性和生长反应。在过度喂养实验中,食物摄入量的测定方式如下:(a)有或没有强制喂食的情况下,以及(b)未接触铅和经口服或全身给予铅的情况下。与对照组相比,铅暴露降低了食物消耗量。强制喂食流质饮食进一步降低了食物消耗量,但仅降至将总热量摄入维持在或接近未强制喂食的铅暴露动物水平。在食物限制实验中,幼鼠的食物摄入量被限制4天,然后给予自由进食,此时这些动物的一个亚组接触铅。在食物消耗和生长方面,之前食物受限的动物在前两天的追赶情况相同,无论是否给予铅。在接下来的10天里,未接触铅、食物受限的动物的食物摄入量和生长逐渐趋近于之前自由进食、未接触铅的动物,而食物受限且接触铅的动物则趋近于生长受抑制、之前自由进食且接触铅的动物。所有这些对饮食操作的反应都与食欲设定点降低一致,而不是与铅的非特异性效应一致,例如对食物的厌恶或全身不适。