Physiological factors responsible for the cessation of eating can be divided into stomach and hormonal factors. Each of these contributes to what is typically referred to as satiety.
Stomach Factors. The stomach produces two types of satiety signal: one associated with the nutrient content of the meal and the other with the volume of the meal (10). It seems likely that these two meal-related signals are detected by separate mechanisms in the gut, because rats can regulate caloric intake independently from meal volume and meal volume can produce satiety cues that do not depend on caloric content.
Nutrient receptors in the stomach respond to the caloric density of a meal. A large but low-calorie meal would activate a large number of nutrient receptors but at a low rate, whereas a small but calorically dense meal would activate a small number of nutrient receptors at a high rate. In addition to this indirect effect on nutrient receptor activation rate, meal volume also induces satiety directly by activating stretch receptors in the stomach.
Current research indicates that stomach distension cues (which activate stretch receptors) and caloric cues (which activate nutrient receptors) are transmitted through separate channels. Stomach distension cues are transmitted to the brain by way of the vagus nerve, whereas stomach nutrient cues do not require the integrity of the vagus nerve and may therefore involve hormonal messengers (10).
Hormonal Factors. Although a number of different hormones have been implicated in satiety, the present discussion will briefly describe the influence of glucagon and cholecystokinin (CCK), the two hormones that have received the most attention as likely satiety agents. Glucagon is produced by islet cells of the pancreas as well as by cells in the gut. Animals treated with glucagon eat smaller than normal meals and animals treated with antibodies to glucagon eat larger than normal meals, suggesting that endogenous glucagon may contribute to meal termination. Because glucagon stimulates the conversion of glycogen (the stored form of glucose that cannot be directly utilized for energy) to glucose, the resultant increased levels of glucose released into the hepatic vein from the liver may stimulate glucose receptors and thereby decrease hunger signals.
Cholecystokinin has also received considerable attention as a signal associated with postprandial satiety (11). CCK is released from the duodenum (the upper portion of the small intestine) when food reaches the stomach. Animal and human studies indicate that systemic administration of CCK inhibits food intake through the normal behavioral sequence that characterizes satiety, without affecting water intake, implying that the behavioral effects of CCK are specific to feeding. Physiological studies indi cate that CCK exerts its inhibitory effects on feeding through activation of vagus nerve input to the brain.
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