Hypothalamic glucose sensing: making ends meet.
Hypothalamic glucose sensing: making ends meet.
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DOI：
10.3389/fnsys.2014.00236
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发表时间：
2014
影响因子：
3
通讯作者：
Zhou C
中科院分区：
文献类型：
--
作者：
Routh VH;Hao L;Santiago AM;Sheng Z;Zhou C
神经内分泌系统控制着基本的生存和自我平衡功能。例如，生长是发育所必需的，体温调节在不断变化的环境中保持最佳核心温度，繁殖确保物种生存。压力和免疫反应使生物体能够克服外部和内部的威胁，而昼夜节律系统调节唤醒和睡眠，使植物和活动功能不会重叠。所有这些功能都需要身体能量的很大一部分。作为神经内分泌系统的整合者，下丘脑仔细评估身体的能量状态，以便适当地分配资源，为每个系统提供而不损害其他系统。在这样做的同时，下丘脑必须确保为大脑功能保留足够的葡萄糖水平，因为葡萄糖是大脑的主要燃料。为此，下丘脑含有专门的葡萄糖传感神经元，其分散在控制不同神经内分泌功能的核团中。我们假设这些神经元在使下丘脑能够分配能量以满足这些外周生存需求而不危及大脑的葡萄糖供应方面起着关键作用。本文将首先介绍下丘脑离散核团内神经元葡萄糖感知的不同机制。然后，我们将评估外周能量状态调节葡萄糖敏感性的方式。例如，在能量缺乏期间，例如禁食，特定的下丘脑葡萄糖感应神经元变得对葡萄糖减少敏感。当葡萄糖可用性对大脑来说是一个更大的关注时，这增加了信息中继的增益。最后，在病理条件下葡萄糖敏感性的变化（例如，复发性胰岛素低血糖症、糖尿病）。这篇综述的总体目标是将葡萄糖敏感神经元置于下丘脑控制神经内分泌功能的背景下。
The neuroendocrine system governs essential survival and homeostatic functions. For example, growth is needed for development, thermoregulation maintains optimal core temperature in a changing environment, and reproduction ensures species survival. Stress and immune responses enable an organism to overcome external and internal threats while the circadian system regulates arousal and sleep such that vegetative and active functions do not overlap. All of these functions require a significant portion of the body's energy. As the integrator of the neuroendocrine system, the hypothalamus carefully assesses the energy status of the body in order to appropriately partition resources to provide for each system without compromising the others. While doing so the hypothalamus must ensure that adequate glucose levels are preserved for brain function since glucose is the primary fuel of the brain. To this end, the hypothalamus contains specialized glucose sensing neurons which are scattered throughout the nuclei controlling distinct neuroendocrine functions. We hypothesize that these neurons play a key role in enabling the hypothalamus to partition energy to meet these peripheral survival needs without endangering the brain's glucose supply. This review will first describe the varied mechanisms underlying glucose sensing in neurons within discrete hypothalamic nuclei. We will then evaluate the way in which peripheral energy status regulates glucose sensitivity. For example, during energy deficit such as fasting specific hypothalamic glucose sensing neurons become sensitized to decreased glucose. This increases the gain of the information relay when glucose availability is a greater concern for the brain. Finally, changes in glucose sensitivity under pathological conditions (e.g., recurrent insulin-hypoglycemia, diabetes) will be addressed. The overall goal of this review is to place glucose sensing neurons within the context of hypothalamic control of neuroendocrine function.