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While central administration of ligands for fibroblast growth factor receptors (FGFRs) such as fibroblast growth factor-19 (FGF19) and FGF21 exert glucose-lowering effects in rodent models of obesity and type 2 diabetes, intracerebroventricular administration of the non-selective FGFR inhibitor PD173074 causes glucose intolerance, implying a physiological role for neuronal FGFR signaling in glucose homeostasis.

Rojas and colleagues extend previous evidence that intracerebroventricular administration of PD173074 impairs glucose tolerance in rats by demonstrating that this effect is associated with, and likely secondary to, a marked but transient sympathoadrenal activation suggestive of an acute stress response. The sympathoadrenal response is rapid in onset but clears rapidly. Acute blockade of central FGFRs impairs glucose tolerance via reductions of both insulin secretion and the basal insulin effect.



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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Flaminia Fanelli
University of Bologna, Italy
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