Journal
CELL METABOLISM
Volume 30, Issue 1, Pages 111-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2019.04.001
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Funding
- National Health and Medical Research Council (NHMRC) [1066809, 1118775]
- Australian Research Council [DP170100063]
- National Health and Medical Research Council of Australia [1118775, 1066809] Funding Source: NHMRC
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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-fatdiet intervention. Central amygdala NPY neuron-specific Npy overexpression mimics the obese phenotype seen in a combined stress and highfat-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.
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