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Unlike endogenous GLP-1, which is rapidly degraded by dipeptidyl peptidase-4, GLP-1 receptor agonists are resistant to degradation and have longer half-lives, particularly for modern long-acting agents, such as liraglutide, dulaglutide, semaglutide and tirzepatide

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The neural pathways involved in GLP-1 receptor-mediated reduction in food intake include feeding centers in the hypothalamus and hindbrain, the mesolimbic reward system (such as the ventral hippocampus), and certain forebrain regions, including the medial prefrontal cortex [14, 15]

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