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In cell experiments, GLP-1 was found to have more mechanisms that may inhibit liver fat synthesis, such as FAM3A, NRF2, NaB, SHP1/AMPK, NLRP3, FGF21, IRS2, and other signaling pathways, which also provided direct evidence for the role of GLP-1R in the regulation of lipid metabolism in the liver

Renal or hepatic impairment necessitates dose and timing adjustments, as these organs are responsible for metabolism and excretion

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While the histological data presented here do not definitively prove the absence of synapses between L-cells and vagal fibers, they contribute to the growing body of literature indicating that enteroendocrine cells primarily communicate through paracrine mechanisms

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trials assessed 12 mg as the highest maintenance dose [1] [3]