Woods Stephen C
Dept. of Psychiatry, Univ. of Cincinnati, Cincinnati, OH 45267, USA.
Am J Physiol Gastrointest Liver Physiol. 2004 Jan;286(1):G7-13. doi: 10.1152/ajpgi.00448.2003.
An overview is presented of those signals generated by the gastrointestinal (GI) tract during meals that interact with the central nervous system to create a sensation of fullness and satiety. Although dozens of enzymes, hormones, and other factors are secreted by the GI tract in response to food in the lumen, only a handful are able to influence food intake directly. Most of these cause meals to terminate and hence are called satiety signals, with CCK being the most investigated. Only one GI signal, ghrelin, that increases meal size has been identified. The administration of exogenous CCK or other satiety signals causes smaller meals to be consumed, whereas blocking the action of endogenous CCK or other satiety signals causes larger meals to be consumed. Satiety signals are relayed to the hindbrain, either indirectly via nerves such as the vagus from the GI tract or else directly via the blood. Most factors that influence how much food is eaten during individual meals act by changing the sensitivity to satiety signals. This includes adiposity signals as well as habits and learning, the social situation, and stressors.
本文概述了进餐期间胃肠道产生的那些与中枢神经系统相互作用以产生饱腹感的信号。尽管胃肠道会响应肠腔内的食物分泌数十种酶、激素和其他因子，但只有少数几种能够直接影响食物摄入量。其中大多数会使进餐终止，因此被称为饱腹感信号，胆囊收缩素（CCK）是研究最多的一种。目前仅确定了一种会增加进餐量的胃肠道信号，即胃饥饿素。给予外源性CCK或其他饱腹感信号会使进餐量减少，而阻断内源性CCK或其他饱腹感信号的作用则会使进餐量增加。饱腹感信号通过迷走神经等神经从胃肠道间接传递至后脑，或者直接通过血液传递。大多数影响个体进餐时食物摄入量的因素通过改变对饱腹感信号的敏感性来起作用。这包括肥胖信号以及习惯、学习、社会环境和应激源。
