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Along these lines, GLP-1-expressing NTS neurons project to the PVT, and administration of exendin-4 into this brain region reduces food intake and motivation for food reward, while exendin-9 has the opposite effect [163]
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To confirm that the observed effects were mediated through direct GLP-1R activation, or indeed, that they are not secondary autocrine effects of insulin, we performed 2-NBDG uptake experiments in the presence of the GLP1R antagonist Exendin (939) and the potassium channel opener, diazoxide
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