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In this enzymatic reaction, GSH becomes oxidized to GSSG, which is recycled back to GSH by the NADPH-dependent GSSG reductase as shown in Figure 2

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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