Appetite Suppression
A reduction in the desire to eat, mediated by hormonal signals and neural circuits in the brain. GLP-1 receptor agonists suppress appetite through activation of GLP-1 receptors in the hypothalamus and brainstem, which are key brain regions for energy balance regulation.
Technical Context
GLP-1 RA appetite suppression involves central and peripheral mechanisms. Central: GLP-1Rs are expressed in hypothalamic appetite centres (arcuate nucleus, paraventricular nucleus), brainstem satiety centres (area postrema, NTS), and reward centres (nucleus accumbens, ventral tegmental area). Semaglutide crosses the BBB (demonstrated in animal studies) and directly activates these GLP-1Rs. Functional MRI studies show reduced activation of food-reward brain regions in semaglutide-treated subjects. Peripheral: vagal afferent GLP-1Rs transmit satiety signals from the gut to the brainstem. The relative contribution of central vs peripheral mechanisms is debated — some evidence suggests central effects dominate for long-acting GLP-1 RAs. Patient-reported outcomes in weight management trials confirm subjective appetite reduction: significantly fewer food cravings, less hunger, and smaller portion sizes.