2019年7月出版的《细胞—干细胞》杂志，发表了澳大利亚加文医学研究所Herbert Herzog研究小组的最新成果。他们发现在压力下，高脂饮食会增加中央杏仁核一种抗焦虑肽NPY的表达，帮我们减压。但NPY会让我们吃的FC碰碰胡老虎机法典-提高赢钱机率的下注技巧，能量消耗减少，造成肥胖。

该课题组研究人员发现了一个未知的喂养刺激途径，是在压力条件下，结合高热量食物激活;杏仁核中央的NPY神经元对压力和高脂肪饮食干预的反应加剧负有责任。中枢杏仁核NPY神经元特异性的NPY过表达与应激和高脂饮食联合模型中的肥胖表型相似，但可通过选择性消融NPY来预防。以食物摄入量和能量消耗为读数，该团队证明了选择性激活中央杏仁核NPY神经元导致食物摄入量增加和能量消耗减少。从机制上讲，正是在压力和高脂肪饮食的共同作用下，中枢杏仁核NPY神经元的胰岛素信号传导能力下降，导致了肥胖的过度发展。

研究人员表示，神经肽Y (NPY)对下丘脑具有很强的促食作用。然而，下丘脑外核也产生NPY，但其对能量稳态的影响尚不清楚。

附：英文原文

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

Author: Chi Kin Ip, Lei Zhang, Aitak Farzi, Ramon Tasan, Günther Sperk, Herbert Herzog

Issue&Volume: Jul 02, 2019 Volume 30Issue 1

Abstract: 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.

DOI: https://doi.org/10.1016/j.cmet.2019.04.001

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(19)30185-8