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2 Previously described as a harmless metabolic byproduct, it is now implicated in the pathogenesis of cardiovascular disease (CVD), chronic kidney disease (CKD), and other metabolic syndromes
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We now demonstrate that GIPR agonist administration critically relies on Gipr expression in the hindbrain, while GIPR antagonism relies on hypothalamic Gipr expression—both are probably neuronal populations, given that we used hSyn-driven Cre-expression for the region-specific knockout studies
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