Satiety control refers to the complex neuroendocrine process that regulates the feeling of fullness and the subsequent suppression of appetite following food consumption, thereby determining the interval until the next meal. This homeostatic mechanism is governed by a sophisticated interplay of gastrointestinal hormones, central nervous system signaling, and stretch receptors in the stomach. Optimal satiety control is a clinical goal for weight management and metabolic health, as its dysregulation often leads to chronic overconsumption and the development of insulin resistance. It is a key physiological determinant of energy balance.
Origin
The term is derived from the Latin word satietas, meaning “fullness” or “enough.” The scientific study of satiety control evolved from early nutritional research into the complex field of gut-brain axis communication and appetite regulation. Modern endocrinology has identified specific peptide hormones that act as key messengers in this system.
Mechanism
The mechanism is primarily mediated by the release of anorexigenic (appetite-suppressing) peptide hormones from the gut, such as Cholecystokinin (CCK), Peptide YY (PYY), and Glucagon-like Peptide-1 (GLP-1), in response to nutrient presence. These hormones travel through the bloodstream and act on receptors in the hypothalamus, particularly the arcuate nucleus, to inhibit the hunger-promoting Neuropeptide Y (NPY) neurons and activate the satiety-promoting Pro-opiomelanocortin (POMC) neurons. This hormonal feedback loop provides the central nervous system with the necessary clarity to terminate feeding behavior.
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