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This rapid neurological effect occurs because the GLP-1 receptor sits in brain regions controlling satiety and food motivation

Specifically, at concentrations of 100 nM and 1,000 nM, GLP-1R agonist 2 significantly enhances 10 mM glucose-induced insulin secretion, similar to GLP-1, and this effect is abolished in islets from GLP-1 receptor knockout mice [2]

In a multivariate regression analysis, FPG levels did not predict T2DM development

Patients who discontinue semaglutide short-term often experience rapid hunger rebound, as their GLP-1 receptor sensitivity returns to pre-treatment levels

fat cells), nor did it negatively affect the enzymes of other metabolic processes