Satiety signaling refers to the entire afferent and efferent communication network that originates from the gastrointestinal tract and adipose tissue, conveying information about nutrient status and energy sufficiency to the central nervous system to terminate a meal and inhibit further food intake. This sophisticated endocrine and neural pathway is the biological mechanism underlying the feeling of satiety. Dysregulation of this signaling cascade is a core contributor to overeating and the pathogenesis of obesity and metabolic syndrome.
Origin
The concept of Satiety Signaling arose from the discovery of specific gut-derived hormones that act on the brain to regulate appetite, linking the physiological state of the gut to central nervous system control. It is a refinement of the broader concept of satiety, focusing on the molecular and neural pathways involved. Key discoveries in the 1990s and 2000s identified the roles of peptides like leptin, ghrelin, and PYY in this complex communication loop.
Mechanism
The signaling cascade begins with the secretion of anorexigenic peptides from enteroendocrine cells in the gut in response to ingested nutrients. These hormones, including GLP-1 and PYY, travel via the bloodstream to cross the blood-brain barrier or activate vagal afferents, ultimately reaching the hypothalamus. In the hypothalamus, these signals promote the release of α-Melanocyte Stimulating Hormone (α-MSH) and inhibit NPY, effectively shifting the balance toward appetite suppression and reduced caloric intake.
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