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Pharmacological inhibition of the PI3K/mTOR pathway abolished such effects, suggesting that the metabolic actions of GLP-1 depend on mTOR activity
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Although our previous research has explored the preliminary mechanisms of EA in the hypothalamus SIRT1-mediated homeostatic feeding and the NTS GLP1 -mediated reward feeding [29, 30], the specificity related to the functional connectivity between neural nuclei and the EA effect has not been deeply probed
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