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An in vitro study using GnRH neurons of adult male mice demonstrated that both GLP-1 and Ex4 might excite GnRH neurons, either directly or indirectly by modulating the nitric oxide (NO) and endocannabinoid pathways that control the presynaptic excitatory GABA-ergic inputs to GnRH neurons [36]

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And the increased synthesis will also drive division of pituicytes that make prolactin, which may eventually result in microadenoma and may eventually result in a macroadenoma (Peki et al., 2019)

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Conclusion This study suggested a bidirectional causal relationship between T2D and SA, with GLP-1-RAs potentially serving as a therapeutic target for SA