Appetite suppression mechanisms encompass the complex physiological and neurochemical processes that lead to the cessation of food seeking and the feeling of satiety. These intricate systems regulate short-term meal termination and long-term energy balance by signaling energy sufficiency to the central nervous system. They involve a coordinated effort between peripheral organs, gut hormones, and the brain’s hypothalamic nuclei. Effective function of these mechanisms is paramount for preventing overconsumption and maintaining a healthy body weight.
Origin
The understanding of appetite control evolved from early theories focused on stomach distension to a sophisticated hormonal and neural network model. The Greek root orexis refers to a desire or appetite, and suppression denotes the act of holding back or inhibiting. The modern clinical definition integrates the action of gut-derived satiety signals, which are key players in these mechanisms.
Mechanism
Satiety signals are initiated by the release of anorexigenic hormones, such as GLP-1, PYY, and CCK, from the gastrointestinal tract in response to nutrient presence. These peptides travel via the circulation and the vagal afferent nerve to the brainstem and hypothalamus. Within the arcuate nucleus of the hypothalamus, these signals stimulate Pro-Opiomelanocortin (POMC) neurons, which release alpha-melanocyte-stimulating hormone (α-MSH). This neurochemical action ultimately inhibits the desire to eat, thereby suppressing appetite.
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