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Comparative metabolic and hepatic effects of GLP-1-based mono-, dual-, and triple-agonist therapies GLP-1 receptor signaling Intestinal L-cells serve as the primary source of GLP-1 synthesis, which operates via G-protein coupled receptors present in pancreatic beta cells, gastrointestinal and central neural systems, cardiac tissues, and kidneys [26]

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This approach is supported by FDA guidance on GLP-1 receptor agonist class labeling for semaglutide in renally impaired patients [11] and by the general pharmacodynamic rationale that slower CNS adaptation reduces nausea burden [10, 12]