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In animal models (and in vitro work), it has been shown to release GH without substantially raising other hormones like ACTH or cortisol, which means less off-target hormonal disturbance

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Treatment with the GIPR antagonist and acyl-GLP-1 both led to a reduction in the likelihood of Nrxn3-Nlgn1 signalling between C35 GABA4 neurons and Pomc.GLU-5 and Agrp.GABA-4 neurons, a change that was specific to these feeding-related neurons and absent in other hypothalamic neurons (Fig

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