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The incretin effect of GLP-1 leads to a marked postprandial increase in circulating levels, which enhances insulin secretion.23,24 Elevated postprandial GLP-1 concentrations may be influenced by mechanical stimuli such as gastric distension,3,25 which also activates GLP-1-expressing neurons in the nucleus tractus solitarius (NTS).26 These responses may involve oxytocin-mediated vagal afferent signaling and contribute to the central GLP-1 systems role in promoting a negative energy balance.27,28 Beyond mechanical stimuli, classical satiety hormones, such as cholecystokinin, augment both central GLP-1 neuronal activity and peripheral GLP-1 release;29 however, the concentrations of cholecystokinin required to stimulate peripheral GLP-1 secretion may exceed physiological levels.30 GLP-1 secretion is modulated by various peptides, neurotransmitters, and nutrients, including carbohydrates, lipids, proteins, and amino acids, highlighting the complexity of its regulatory mechanisms.3,31 GLP-1 exerts its effects via the G-protein-coupled receptor,32,33 which is expressed on pancreatic beta cells as well as neurons within the central and peripheral nervous systems

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