The past 15 years has witnessed unprecedented growth in our understanding of the neural and neuroendocrine systems that regulate energy homeostasis. In addition to upholding many of the predictions made prior to this period, the field has elucidated hormones, circuits, and processes that contribute to energy balance, and has identified new hypotheses, dilemmas, and predictions to be examined in the near future. The modulation by energy status of variables that govern energy intake (eating) and expenditure have been understood for some time: Animals and humans undergoing caloric restriction exhibit increased “craving” for food (especially calorically dense food) and diminished satiety, promoting increased feeding (Schwartz et al., 2000). Undernourishment simultaneously provokes increased metabolic efficiency, decreased locomotor activity, and diminished activity in endocrine axes (e.g., thyroid, gonadotropic, etc.) that require energy utilization (Ahima et al., 2000). Equally important, overfeeding and acute weight gain decrease feeding and increase parameters of energy expenditure, promoting the rebound of energy stores toward their baseline status (Rosenbaum et al., 2002; Schwartz et al., 2000).

中文翻译：

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能量平衡的神经内分泌学和神经科学

在过去的 15 年里，我们对调节能量稳态的神经和神经内分泌系统的理解取得了前所未有的增长。除了支持这一时期之前的许多预测外，该领域还阐明了有助于能量平衡的激素、回路和过程，并确定了新的假设、困境和预测，以在不久的将来进行检查。一段时间以来，人们已经了解了能量状态对控制能量摄入（进食）和支出的变量的调节：限制热量的动物和人类表现出对食物（尤其是热量密集的食物）的“渴望”增加和饱腹感减少，从而促进了进食的增加。施瓦茨等人，2000 年）。营养不良同时会引起代谢效率的提高、运动能力的降低、需要能量利用的内分泌轴（例如甲状腺、促性腺激素等）的活动减弱（Ahima 等，2000）。同样重要的是，过度喂养和急性体重增加会减少喂养并增加能量消耗参数，促进能量储存向基线状态反弹（Rosenbaum 等人，2002 年；Schwartz 等人，2000 年）。