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Combined with above-mentioned data, GLP-1RAs show a positive impact on the suppression of NLRP3 inflammasome (Figure 2)

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[1] [3] Once released, GLP-1 does several well-characterized things

The receptor-independent passive access theory presented by Kastin and colleagues [88,89] challenges the classical dogma that BBB only allows its paracellular access of molecules that are smaller than 500 Da, while native gut-produced GLP-1 and GLP-1RA therapeutic agents are much larger than 3000 Da

Intra-accumbens amphetamine increases the conditioned incentive salience of sucrose reward: enhancement of reward wanting without enhanced liking or response reinforcement