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NPY mediates the rapid feeding and glucose metabolism regulatory functions of AgRP neurons.

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Fenselau,  Henning
Fenselau – Synaptic Transmission in Energy Homeostasis, Research Groups, Max Planck Institute for Metabolism Research, Max Planck Society;

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Brüning,  Jens C.
Brüning – Neuronal Control of Metabolism, Department Brüning, Max Planck Institute for Metabolism Research, Max Planck Society;

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Citation

Engström Ruud, L., Pereira, M. M. A., de Solis, A. J., Fenselau, H., & Brüning, J. C. (2020). NPY mediates the rapid feeding and glucose metabolism regulatory functions of AgRP neurons. Nature communications, (1).


Cite as: https://hdl.handle.net/21.11116/0000-000C-7611-C
Abstract
Activation of Agouti-Related Peptide (AgRP)-expressing neurons promotes feeding and insulin resistance. Here, we examine the contribution of neuropeptide Y (NPY)-dependent signaling to the diverse physiological consequences of activating AgRP neurons. NPY-deficient mice fail to rapidly increase food intake during the first hour of either chemo- or optogenetic activation of AgRP neurons, while the delayed increase in feeding is comparable between control and NPY-deficient mice. Acutely stimulating AgRP neurons fails to induce systemic insulin resistance in NPY-deficient mice, while increased locomotor activity upon AgRP neuron stimulation in the absence of food remains unaffected in these animals. Selective re-expression of NPY in AgRP neurons attenuates the reduced feeding response and reverses the protection from insulin resistance upon optogenetic activation of AgRP neurons in NPY-deficient mice. Collectively, these experiments reveal a pivotal role of NPY-dependent signaling in mediating the rapid feeding inducing effect and the acute glucose regulatory function governed by AgRP neurons.