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Amygdala NPY Circuits Promote the Development of Accelerated Obesity under Chronic Stress Conditions


Neuropeptide Y (NPY) exerts a powerful orexigenic effect in the hypothalamus. However, extra-hypothalamic nuclei also produce NPY, but its influence on energy homeostasis is unclear. Here we uncover a previously unknown feeding stimulatory pathway that is activated under conditions of stress in combination with calorie-dense food; NPY neurons in the central amygdala are responsible for an exacerbated response to a combined stress and high-fat-diet intervention. Central amygdala NPY neuron-specific Npy overexpression mimics the obese phenotype seen in a combined stress and high-fat-diet model, which is prevented by the selective ablation of Npy. Using food intake and energy expenditure as readouts, we demonstrate that selective activation of central amygdala NPY neurons results in increased food intake and decreased energy expenditure. Mechanistically, it is the diminished insulin signaling capacity on central amygdala NPY neurons under combined stress and high-fat-diet conditions that leads to the exaggerated development of obesity.

Type Journal
ISBN 1932-7420 (Electronic) 1550-4131 (Linking)
Authors Ip, C. K.; Zhang, L.; Farzi, A.; Qi, Y.; Clarke, I.; Reed, F.; Shi, Y. C.; Enriquez, R.; Dayas, C.; Graham, B.; Begg, D.; Bruning, J. C.; Lee, N. J.; Hernandez-Sanchez, D.; Gopalasingam, G.; Koller, J.; Tasan, R.; Sperk, G.; Herzog, H.
Responsible Garvan Author Prof Herbert Herzog
Publisher Name Cell Metabolism
Published Date 2019-04-25
Published Volume 30
Published Issue 1
Published Pages 111-128
Status Published in-print
DOI 10.1016/j.cmet.2019.04.001
URL link to publisher's version
OpenAccess link to author's accepted manuscript version