Smythe G A, Grunstein H S, Bradshaw J E, Nicholson M V, Compton P J
Nature. 1984;308(5954):65-7. doi: 10.1038/308065a0.
Glucose is the principal energy substrate for the brain and studies have shown that the brain is able to increase glucose availability in the face of glucose starvation (neuroglycopaenia). The mechanisms, believed to be hypothalamic, that may be involved in a brain/blood glucose control system have not yet been identified. We have used novel techniques for assessing brain monoamine neuronal activity to investigate its relationship to blood glucose concentrations in the rat. We describe here two important relationships which emerge from these studies. One is that activation of hypothalamic noradrenaline (NA) activity following stress is associated with concurrent increases in plasma glucose concentrations. This relationship is linear and independent of the adrenal or pituitary glands. The second is an inverse relationship between plasma glucose concentration and hypothalamic NA neuronal activity--high blood glucose levels significantly inhibited the hypothalamic NA activity responses to stress, alpha 2-adrenergic blockade and adrenalectomy. Thus glucose (or a metabolite of it) seems to provide a negative feedback signal sensed by hypothalamic NA neuronal systems which, in turn, appear to stimulate liver glucose output by a neural mechanism.
葡萄糖是大脑的主要能量底物,研究表明,面对葡萄糖饥饿(神经低血糖症)时,大脑能够增加葡萄糖的可利用性。据信,可能参与大脑/血糖控制系统的机制位于下丘脑,但尚未确定。我们使用了评估脑单胺神经元活性的新技术来研究其与大鼠血糖浓度的关系。我们在此描述这些研究中出现的两个重要关系。一是应激后下丘脑去甲肾上腺素(NA)活性的激活与血浆葡萄糖浓度的同时升高有关。这种关系是线性的,且独立于肾上腺或垂体。二是血浆葡萄糖浓度与下丘脑NA神经元活性之间呈负相关——高血糖水平显著抑制下丘脑NA活性对应激、α2-肾上腺素能阻断和肾上腺切除术的反应。因此,葡萄糖(或其代谢物)似乎提供了一种由下丘脑NA神经元系统感知的负反馈信号,而该系统反过来似乎通过神经机制刺激肝脏葡萄糖输出。