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Assuming a preferential central action of GLP1/E, we conducted label-free, quantitative proteomic analyses in the hypothalamus of the two models of PCOS, after chronic treatment with the di-agonist, as a means to disclose putative pathways for the metabolic actions of the di-agonist, and the basis for the partially differential responses between the two models of PCOS, which diverge also in terms of phenotypic presentation