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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

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The activation of the GIP receptor in the arcuate, dorsomedial and paraventricular nuclei of the hypothalamus decreased food intake in obese mice

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Acknowledgements Thanks are given to Christian Tikkanen and Pierre Johansen, from Novo Nordisk, for reviewing model assumptions and providing feedback on a draft manuscript