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GLP-1 Receptor Pathway - Reduces hunger drive centrally (hypothalamus, brainstem) - Decreases the reward value of food (mesolimbic system) - Enhances glucose-dependent insulin secretion - Slows gastric emptying Amylin Receptor Pathway - Induces satiety through the area postrema and NTS - Activates POMC neurons (pro-satiety) and suppresses NPY/AgRP neurons (pro-hunger) in the arcuate nucleus - Additional gastric emptying delay through distinct neural circuits - Suppresses post-prandial glucagon secretion - May contribute to leptin resensitization The combination of these two pathways produces what researchers describe as broader modulation of neuroendocrine appetite control — meaning amycretin hits more of the biological “switches” that drive eating behavior than a GLP-1-only drug can reach

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SA-β-gal staining demonstrated a notable reduction in the number of SA-β-gal-positive cells post-FOXO4-DRI treatment compared to the PBS group (Figure 4D)