A study of the effect of limitation of food intake and the method of feeding on the rate of weight gain during hypothalamic obesity in the albino rat.
A study of the effect of limitation of food intake and the method of feeding on the rate of weight gain during hypothalamic obesity in the albino rat.
复制标题
限制食物摄入量和喂养方法对白化大鼠下丘脑肥胖期间体重增加率影响的研究。
DOI：
10.1152/ajplegacy.1946.147.4.695
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发表时间：
1946
期刊：
影响因子：
--
通讯作者：
E. F. Lambert
中科院分区：
文献类型：
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作者：
C. Brooks;E. F. Lambert
多年来人们都知道肥胖可能是由于下丘脑损伤引起的 (7)。此外，通过在大脑该区域的特定区域造成损伤，在不同种类的动物中实验性地产生了肥胖(1,2,8,13)。人们已经进行了许多尝试来确定这些引起肥胖的病变所造成的不平衡的性质(3,11)，但许多问题仍然没有得到解答。这种研究中出现的主要问题是确定通常维持食物摄入和能量利用之间平衡的机制失效的原因。因此，在本次调查中，我们试图发现一些可能导致不平衡的异常现象，并评估它们的相对重要性。后续论文将讨论该问题的其他方面。肥胖可分为两个阶段，体重快速增加的动态阶段和体重没有异常增加但维持肥胖状态的静态阶段。在后一个阶段，显然在增加和减少肥胖的因素之间重新建立了平衡。因此，似乎可以合理地假设，在可能消除或掩盖缺陷的重新调整发生之前，在动态阶段最容易检测到导致肥胖的不平衡的本质。导致肥胖动态阶段终止以及随着衰老的发展而最终发生的体重减轻的因素必须与那些造成肥胖状况的因素相反。这种通过实验产生的肥胖可能是由于食欲不振、饱腹感丧失、消化系统效率改变、新陈代谢降低或活动水平降低而导致能量输出减少而食物摄入量没有相应减少，或者是这些因素和其他致病因素的组合。已经尝试确定这些各种可能的影响因素是否起作用。本文总结的部分研究涉及受食物摄入限制和喂养方法影响的体重增加率。虽然我们的许多实验产生的数据只是放大和支持以前在其他实验室所做的工作，但人们认为我们的研究
It has been known for many years that obesity may develop as a result of injury to the hypothalamus (7). Furthermore, obesity has been produced experimentally in various species of animals by making lesions in specific areas of this region of the brain (1,2,8,13). Numerous attempts to determine the nature of the imbalance created by these obesity producing lesions (3,11) have been made, but many questions still remain unanswered. The principal problem which presents itself in such a study is that of determining the cause of the failure of mechanisms which normally maintain the balance between food intake and energy utilization. Consequently, in the present investigation we attempted to detect some of the abnormalities which might contribute to the imbalance and evaluate their relative importance. Subsequent papers will deal with other aspects of this problem. Obesity can be divided into two phases, a dynamic phase during which weight is gained at a rapid rate and a static phase during which there is no abnormal gain but the obese condition is maintained. In this latter phase apparently a balance is re-established between factors tending to increase and decrease the obesity. It seemed reasonable to assume, therefore, that the nature of the imbalance which causes the obesity could be detected most readily during the dynamic phase before readjustments occur which might abolish or mask the defects. The factors responsible for the termination of the dynamic phase of obesity and for the weight loss which eventually occurs as senescence develops must act in opposition to those which create the obese condition. This experimentally produced obesity might be due to an increase inappetite, to a failure of the sense of satiety, to a change in the efficiency of the digestive system, to a decrease in energy output resulting from a lowered metabolism or a lowered level of activity without a corresponding decrease in food intake, or to a combination of these and other causative factors. Attempts have been made to determine whether or not these various possible contributory factors do operate. The portion of this study which is summarized in this paper deals with the rate of weight gain as affected by limitations of food intake and the method of feeding. While many of our experiments have produced data which merely amplify and support work previously done in other laboratories, it is thought that our studies