Satiety Hormone Signaling refers to the complex neuroendocrine communication network by which peripheral hormones released from the gastrointestinal tract and adipose tissue transmit messages of fullness to the central nervous system, primarily the hypothalamus. Key hormonal messengers involved include leptin, cholecystokinin (CCK), peptide YY (PYY), and glucagon-like peptide-1 (GLP-1). This intricate signaling cascade is fundamental to the homeostatic regulation of appetite, energy balance, and the maintenance of a stable body weight. Efficient signaling ensures appropriate termination of food intake and the long-term equilibrium of energy stores.
Origin
This term is rooted in the fields of endocrinology and neuroendocrinology, specifically the study of the gut-brain axis and adipokine regulation. The use of the word signaling emphasizes the communicative and dynamic nature of the process, which relies on molecular messengers and their specific receptors. Understanding this complex mechanism has been transformative in obesity and metabolic research.
Mechanism
Following nutrient ingestion, gut enteroendocrine cells rapidly release peptides like CCK and PYY, which travel via the bloodstream and vagus nerve to the brainstem and hypothalamus, providing short-term satiety cues. Long-term energy status is communicated by leptin, secreted by adipocytes, which binds to receptors in the arcuate nucleus of the hypothalamus to modulate the expression of appetite-regulating neuropeptides. This dual-layered signaling ensures both meal-to-meal and long-term energy homeostasis is maintained.
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