Houpt K A
Neurosci Biobehav Rev. 1982 Summer;6(2):145-64. doi: 10.1016/0149-7634(82)90052-5.
The evidence for the participation of signals from the gastrointestinal tract in hunger and satiety is reviewed. Various methods of subjecting only certain portions of the gastrointestinal tract to food are described including sham feeding, crossing of the intestines of two animals, and intragastric, intraduodenal and intravenous feeding. These methods have revealed that animals eat more when only the mouth is exposed to food, but consume less when food enters the stomach directly and still less when feeding themselves intravenously. The role of the stomach in satiety is discussed in relation to the results of the many experiments in which intragastric loads were administered. These experiments generally revealed that gastric loads suppressed intake in proportion to their caloric value, but that compensation was not precise. A similar analysis is made of the role of the intestines in satiety. These studies present evidence for osmoreceptors and glucoreceptors, distention, and pressure, all of which may participate in satiety. The numerous effects of vagotomy on food intake are reviewed and an attempt is made to separate afferent from efferent effects and vagal effects from nonspecific surgical injury. The role of other afferents is explored. A brief survey of the most recent studies on humoral factors indicates that cholecystokinin is probably acting as a satiety agent, but its mode of action remains unknown. The changes in the gastrointestinal tract that accompany an increase or decrease in food intake reveal adaptive changes that occur in the organ. The evidence for gastrointestinal factors in satiety of the suckling animal is presented. Finally, a hypothesis is presented in which the various factors that bring a meal to an end are included. Preabsorptive satiety may consist of multiple factors which probably include signals from osmoreceptors and possibly other chemoreceptors in the upper small intestine. The signals from these receptors are neural while other products of digestion stimulate the release of humoral agents, such as cholecystokinin, which may act locally, in the liver, or on the central nervous system. Stretch or distention of the intestines at various locations may also contribute to preabsorptive satiety.
本文综述了胃肠道信号参与饥饿和饱腹感调节的相关证据。介绍了仅使胃肠道特定部分接触食物的各种方法，包括假饲、两只动物肠道交叉、胃内、十二指肠内和静脉内喂食。这些方法表明，仅口腔接触食物时动物吃得更多，但食物直接进入胃时摄入量减少，静脉内自我喂食时摄入量更少。结合许多给予胃内负荷实验的结果，讨论了胃在饱腹感中的作用。这些实验通常表明，胃内负荷按其热量值抑制摄入量，但补偿并不精确。对肠道在饱腹感中的作用进行了类似分析。这些研究提供了关于渗透压感受器、葡萄糖感受器、扩张和压力的证据，所有这些都可能参与饱腹感调节。综述了迷走神经切断术对食物摄入的多种影响，并试图区分传入和传出效应以及迷走神经效应与非特异性手术损伤的影响。探讨了其他传入神经的作用。对体液因素最新研究的简要综述表明，胆囊收缩素可能作为一种饱腹感因子起作用，但其作用方式尚不清楚。食物摄入量增加或减少时胃肠道的变化揭示了该器官发生的适应性变化。介绍了幼小动物饱腹感中胃肠道因素的证据。最后，提出了一个假说，其中包括导致一餐结束的各种因素。吸收前饱腹感可能由多种因素组成，可能包括来自渗透压感受器以及可能来自小肠上段其他化学感受器的信号。这些感受器发出的信号是神经性的，而其他消化产物则刺激体液因子如胆囊收缩素的释放，胆囊收缩素可能在局部、肝脏或中枢神经系统起作用。肠道不同部位的伸展或扩张也可能有助于吸收前饱腹感。
