Satiety Hormone Dysfunction describes a pathological state where the regulatory signaling of hormones responsible for inducing the feeling of fullness, or satiety, is impaired, leading to dysregulated energy intake and potential weight gain. This dysfunction can manifest as an inadequate post-prandial secretion of gut-brain peptides like PYY and GLP-1, or, more commonly, as a state of receptor insensitivity or resistance to the adipokine hormone leptin. This impairment disrupts the crucial homeostatic feedback loop that balances energy consumption with energy expenditure. Clinical intervention focuses on restoring the sensitivity and proper communication of this essential endocrine signaling system.
Origin
The term combines satiety hormone, referring to the peptides and adipokines that signal fullness, with dysfunction, indicating impaired operation or communication. It is a concept central to the pathophysiology of obesity and metabolic syndrome, recognizing that weight regulation is fundamentally a complex hormonal and neurological process. This understanding has driven the development of novel pharmacological agents targeting these specific pathways.
Mechanism
The dysfunction often begins at the level of the target receptor, particularly within the appetite-regulating centers of the hypothalamus. Chronic over-nutrition and inflammation can induce leptin resistance, meaning the brain fails to register the signal of adequate energy stores, leading to persistent hunger. Similarly, reduced post-prandial release of gut peptides diminishes the immediate, short-term signal to terminate food intake. This impaired signaling mechanism results in a persistent drive to consume calories despite adequate or excess energy reserves.
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