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

Linda Engström Ruud, Mafalda M. A. Pereira, Alain J. Solis, Henning Fenselau and Jens C. Brüning ()
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Linda Engström Ruud: Max Planck Institute for Metabolism Research
Mafalda M. A. Pereira: Max Planck Institute for Metabolism Research
Alain J. Solis: Max Planck Institute for Metabolism Research
Henning Fenselau: University of Cologne
Jens C. Brüning: Max Planck Institute for Metabolism Research

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: 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.

Date: 2020
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DOI: 10.1038/s41467-020-14291-3

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