近日出版的《细胞—代谢》（Cell Metabolism）杂志刊出，一个人在节食的时候，他的脑细胞也在节食。这些饥饿的脑细胞会释放“我要吃东西”的信号加速饥饿，并使新陈代谢放慢，导致减肥前功尽弃。
此项研究的参与者，纽约市布朗克斯区的爱因斯坦医学院的RajatSingh说：“我们培育了一批大脑不能发出饥饿信号的老鼠，它们的神经元中缺少产生增加食欲的蛋白，研究发现这些老鼠在挨饿后吃得少了，更瘦也更健康了。这些神经元能感应身体中的营养状况，告诉身体是吃东西还是不要吃东西。”
由这些神经元产生的饥饿机制和饥饿感通过一个叫自噬的过程发出信号。大多数脑细胞自噬的时候都保持稳定的水平，不会对饥饿有所反应。而食欲感应神经元不同，它是唯一已知的在饥饿的时候加强自噬过程的脑细胞。加强后的自噬过程增加了游离脂肪酸的细胞水平，而这更高水平的脂肪酸让这些特别的脑细胞分子释放出产生食欲的老鼠基因相关蛋白。因为老鼠基因相关蛋白只在食欲控制神经元中释放，阻止这一过程只会影响食欲信号，不会影响身体其他部位的细胞分解和储存能量的使用。
Singh称，这一发现很可能可应用于人类，对治疗肥胖症有巨大的意义。（生物谷 Bioon.com）
doi:10.1016/j.cmet.2011.06.008
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Autophagy in Hypothalamic AgRP Neurons Regulates Food Intake and Energy Balance
Susmita Kaushik1, 5, Jose Antonio Rodriguez-Navarro1, 5, Esperanza Arias1, 5, Roberta Kiffin1, 5, Srabani Sahu1, 3, Gary J. Schwartz1, 4, 6, Ana Maria Cuervo1, 2, 5, 6 and Rajat Singh
Macroautophagy is a lysosomal degradative pathway that maintains cellular homeostasis by turning over cellular components. Here we demonstrate a role for autophagy in hypothalamic agouti-related peptide (AgRP) neurons in the regulation of food intake and energy balance. We show that starvation-induced hypothalamic autophagy mobilizes neuron-intrinsic lipids to generate endogenous free fatty acids, which in turn regulate AgRP levels. The functional consequences of inhibiting autophagy are the failure to upregulate AgRP in response to starvation, and constitutive increases in hypothalamic levels of pro-opiomelanocortin and its cleavage product α-melanocyte-stimulating hormone that typically contribute to a lean phenotype. We propose a conceptual framework for considering how autophagy-regulated lipid metabolism within hypothalamic neurons may modulate neuropeptide levels to have immediate effects on food intake, as well as long-term effects on energy homeostasis. Regulation of hypothalamic autophagy could become an effective intervention in conditions such as obesity and the metabolic syndrome.
