In addition to various psychosocial and metabolic factors, food intake is also influenced by gastrointestinal mechanisms that trigger both the initiation and termination of eating behaviors. Although gastric distension is one of the most obvious signs of "fullness" and clearly plays a role in controlling food intake, its effects are only temporary and are distinct from the feelings of satiety generally associated with a meal. Such postprandial sensations appear to be related to the activation of intestinal chemoreceptors. Other evidence indicates that the release of cholecystokinin and perhaps other transmitters as well may contribute to satiety. Although the stomach probably does not expand or shrink in response to different levels of food intake, nutrient receptors in the small intestine probably do adapt to changes in food intake. Intestinal adaptation also occurs in response to thyroid hormone, insulin, and cortisol as well as to obesity, pregnancy, and illness, which all may have an important bearing on changes in eating behavior in these situations.