For the GLP-1 receptor activity is slightly lower than natural GLP-1, but this is compensated by the dual mechanism [1]
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This is achieved through stimulation of pro-opiomelanocortin/cocaine- and amphetamine-regulated transcript (POMC/CART) neurons and the indirect inhibition of the orexigenic neuropeptide Y/agouti-related peptide (NPY/AgRP) axis via GABAergic mechanisms.18 The partial permeability of the bloodbrain barrier in circumventricular structures and the arcuate nucleus, alongside potential GLP-1R-dependent involvement of tanycytes, facilitates the access of both LIRA and SEMA to brain regions that are essential in the regulation of food intake
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A rise in cortisol levels would result in mood swings
