Grill Harvey J
Graduate Group of Psychology, University of Pennsylvania, Philadelphia, PA 19104, USA.
Obesity (Silver Spring). 2006 Aug;14 Suppl 5:216S-221S. doi: 10.1038/oby.2006.312.
Data are reviewed that support the hypothesis that the neural control of energy expenditure is distributed among several brain sites. This view contrasts with that expressed most commonly in literature, that a single site-the arcuate hypothalamic nucleus-receives and integrates signals of relevance to energy status assessment and engages the effector circuits that orchestrate responses that maintain energy balance. The data reviewed support a contribution from medullary neurons, including those of the nucleus of the solitary tract, in the integration of signals of relevance to energy balance and in the issuing of commands to local behavioral and autonomic effectors. Experimental evidence is discussed that supports the following specific conclusions: hindbrain neurons integrate oral and gastrointestinal signals and issue commands to local motor circuits that control meal size; leptin's effect on food intake may be mediated, in part, by a direct action on the hindbrain neurons that respond to gastric distention; deprivation signals, such as the fall in leptin level, affect gene expression outside of the hypothalamus with reductions in proglucagon and proopiomelanocortin message seen in nucleus of the solitary tract-rich tissue; and that hindbrain neurons contribute to the control of energy expenditure seen with food deprivation and increases in expenditure after cold exposure or starvation. Future work is needed to define how the nucleus of the solitary tract and arcuate nodes of the central energy balance control network interact to collectively, or separately, influence specific aspects of energy balance control in the intact brain.
现有数据支持这样一种假说，即能量消耗的神经控制分布于多个脑区。这一观点与文献中最常表达的观点形成对比，后者认为单一脑区——弓状下丘脑核——接收并整合与能量状态评估相关的信号，并激活协调维持能量平衡反应的效应器回路。所回顾的数据支持延髓神经元的作用，包括孤束核的神经元，它们参与整合与能量平衡相关的信号，并向局部行为和自主效应器发出指令。文中讨论了支持以下具体结论的实验证据：后脑神经元整合口腔和胃肠道信号，并向控制进食量的局部运动回路发出指令；瘦素对食物摄入的影响可能部分是通过直接作用于对胃扩张有反应的后脑神经元来介导的；诸如瘦素水平下降等剥夺信号会影响下丘脑以外的基因表达，在富含孤束核的组织中可见胰高血糖素原和阿片-促黑素皮质素原信息减少；并且后脑神经元有助于控制禁食时的能量消耗以及冷暴露或饥饿后能量消耗的增加。未来需要开展研究来确定孤束核与中央能量平衡控制网络的弓状核如何相互作用，以共同或分别影响完整大脑中能量平衡控制的特定方面。
