How and why do gastrointestinal peptides influence food intake?

• Published in: Physiology & behavior 2018-09, Vol.193 (Pt B), p.218-222
• Main Authors: Woods, Stephen C., May-Zhang, Aaron A., Begg, Denovan P.
• Format: Article
• Language: English
• Subjects: Animals; Eating - physiology; Gastrointestinal Hormones - metabolism; Humans; Peptides - metabolism; Satiation - physiology
• ISSN: 0031-9384; 1873-507X
• DOI: 10.1016/j.physbeh.2018.02.048

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. •Individual GI peptides are sufficient but not necessary to elicit satiation.•Genetic models do not support the hypothesis that endogenous GI peptides are necessary for maintenance of body weight.•The anorectic action of exogenous CCK is reduced when its repeated administration is dissociated from consumed calories.•Converging data support the hypothesis that GI peptides elicit satiation as a result of classical conditioning.