Woods Stephen C, May-Zhang Aaron A, Begg Denovan P
Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati, United States.
Department of Medicine, Vanderbilt University, Nashville, TN, United States.
Physiol Behav. 2018 Sep 1;193(Pt B):218-222. doi: 10.1016/j.physbeh.2018.02.048. Epub 2018 Mar 22.
Despite the ability of some gastrointestinal hormones to reliably reduce meal size when administered prior to a meal, it is not understood why the repeated administration or genetic knockout of these hormones appear largely ineffective in reducing food intake and body weight. Here, we review evidence that the ability of GI peptides such as cholecystokinin (CCK) to elicit satiation is a consequence of prior learning. Evidence includes first, that the ability of some of these signals to modify food intake depends upon past experience and is malleable with new experience. Additionally, the ability of CCK and other gut signals to reduce food intake may not be hard-wired; i.e., any so-called "satiation" signal that reduces food intake in a single-meal situation may not continue to do so over repeated trials. The individual will respond to the signal only so long as it provides reliable information about caloric content. If a particular signal becomes unreliable, the individual will rely on other signals to end meals. Thus, gut peptides/hormones have important metabolic effects such as mediating absorption, digestion, and many aspects of the distribution of ingested nutrients throughout the body; and, if they have been reliably associated with natural stimuli that mediate satiation, they also inform behavior.
尽管某些胃肠激素在餐前给药时能够可靠地减少进食量，但目前尚不清楚为何重复给药或基因敲除这些激素在减少食物摄入量和体重方面似乎大多无效。在此，我们回顾了相关证据，即胆囊收缩素（CCK）等胃肠肽引发饱腹感的能力是先前学习的结果。证据包括：首先，其中一些信号改变食物摄入量的能力取决于过去的经验，并且会随着新经验而变化。此外，CCK和其他肠道信号减少食物摄入量的能力可能并非固定不变；也就是说，在单餐情况下减少食物摄入量的任何所谓“饱腹感”信号，在重复试验中可能不会继续如此。个体仅在该信号提供有关热量含量的可靠信息时才会对其做出反应。如果某个特定信号变得不可靠，个体将依靠其他信号来结束进食。因此，胃肠肽/激素具有重要的代谢作用，例如介导吸收、消化以及摄入营养物质在全身分布的许多方面；而且，如果它们与介导饱腹感的自然刺激可靠相关，它们也会影响行为。
