Peptides in the gastrointestinal tract and brain are believed to play an important role in the body's decision to commence and conclude meal consumption. When a meal is being consumed, these peptides are secreted by the gut to indicate the level of satiety. Some of this information can be used by the brain to determine the feeling of fullness, in turn influencing the decision to cease consumption. Cholecystokinin (CCK), a polypeptide located in the peripheral and central nervous systems, is one such satiety signal. It is released in proportion to the amount of food being consumed and helps to determine the amount consumed. Following a meal, CCK is secreted from muco-sal epithelial cells in the first segment of the duodenum and stimulates the delivery of digestive enzymes from the pancreas, as well as bile from the gallbladder, into the small intestine. In addition, CCK is produced by neurons in the enteric nervous system and is widely distributed in the brain. The exogenous administration of CCK (and CCK-8, its synthetic analogue) has been shown to influence the amount of food consumed in proportion to the dose given. Although CCK (and other satiety signals) acts to limit meal size, it is important to note that it has little effect on body fat stores, meaning that it does not take into consideration the existing adiposity of the individual when signaling the onset of satiety. Therefore, adiposity signals must be considered in parallel because they also play a part in the process of determining meal size.
Adiposity signals such as leptin act in conjunction with satiety signals in the brain during digestion and their concentration is determined in relation to the degree of adiposity. Like CCK, the effect on meal consumption and body weight of their exogenous administration is dose dependent. Leptin is a peptide hormone produced predominantly by adipocytes, and it is also secreted by the epithelial cells of the stomach. The definitive role of leptin in digestive physiology is still being determined, but it is thought to play a part in limiting food intake in conjunction with CCK. It is when the adiposity signals interact with, and influence, the satiety signals originating from the gut that an attempt at controlling energy intake and meal size is made.
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