Hypothalamic neuronal histamine: Implications of its homeostatic control of energy metabolism
Hypothalamic neuronal histamine: Implications of its homeostatic control of energy metabolism
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DOI：
10.1016/s0899-9007(97)91277-6
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发表时间：
1997-05-01
期刊：
影响因子：
4.4
通讯作者：
Kurokawa, M
中科院分区：
文献类型：
--
作者：
Sakata, T;Yoshimatsu, H;Kurokawa, M
在一系列关于下丘脑组胺能功能的研究中，使用非肥胖正常和Zucker肥胖大鼠（一种遗传性肥胖动物模型），应用操纵组胺能神经元系统活动的探针来评估其生理和病理生理意义。食物摄入通过激活下丘脑腹内侧核（VMH）或室旁核中的H-1受体或抑制H-3受体而被抑制，其中每一个都参与饱腹感调节。中脑三叉神经感觉核中的组胺神经元通过中脑三叉神经运动核调节咀嚼功能，特别是进食速度，并且VMH中的组胺神经元的激活抑制进食时的摄入量。大脑中的能量缺乏，即，神经元内葡萄糖缺乏激活下丘脑中的神经元组胺。这种低能量摄入反过来又加速星形胶质细胞中的糖原分解，以防止大脑能量不足。因此，咀嚼和低能量摄入都作为激活下丘脑中组胺能神经系统的传入信号，并导致饱足感的增强。极低热量的传统日本饮食作为减肥的治疗工具是有效的。摄食昼夜节律是通过操纵下丘脑组胺神经元来调节的。环境温度升高会激活下丘脑组胺神经元。下丘脑神经元组胺控制适应性行为，包括减少食物摄入量和体温，以及增加水摄入量以维持体温正常恒定。此外，白细胞介素-lp，一种内源性热原，通过脑中的前列腺素E-2增强神经元组胺的周转。总之，下丘脑中的组胺神经元系统通过直接和间接控制适应性行为，对维持体温调节至关重要。肥胖Zucker大鼠的行为和代谢异常，包括摄食过多、摄食昼夜节律破坏、高脂血症、高胰岛素血症和体温调节障碍，基本上是由下丘脑神经元组胺缺陷引起的。正常大鼠下丘脑中神经元组胺的耗竭产生的abbrachial与肥胖大鼠相似。将瘦的Zucker胎儿下丘脑移植到肥胖的Zucker幼崽中可以减轻这些异常。这些发现表明，大脑中的组胺神经系统在维持体内能量平衡方面起着至关重要的作用。(C)Elsevier Science Inc. 1997.
In a series of studies on histaminergic functions in the hypothalamus, probes to manipulate activities of histaminergic neuron systems were applied to assess its physiologic and pathophysiologic implications using non-obese normal and Zucker obese rats, an animal model of genetic obesity. Food intake is suppressed by either activation of H-1-receptor or inhibition of the H-3-receptor in the ventromedial hypothalamus (VMH) or the paraventricular nucleus, each of which is involved in satiety regulation. Histamine neurons in the mesencephalic trigeminal sensory nucleus modulate masticatory functions, particularly eating speed through the mesencephalic trigeminal motor nucleus, and activation of the histamine neurons in the VMH suppress intake volume of feeding at meals. Energy deficiency in the brain, i.e., intraneuronal glucoprivation, activates neuronal histamine in the hypothalamus. Such low energy intake in turn accelerates glycogenolysis in the astrocytes to prevent the brain from energy deficit. Thus, both mastication and low energy intake act as afferent signals for activation of histaminergic nerve systems in the hypothalamus and result in enhancement of, satiation. There is a rationale for efficacy of a very-low-calorie conventional Japanese diet as a therapeutic tool for weight reduction. Feeding circadian rhythm is modulated by manipulation of hypothalamic histamine neurons. Hypothalamic histamine neurons are activated by an increase in ambient temperature. Hypothalamic neuronal histamine controls adaptive behavior including a decrease in food intake and ambulation, and an increase in water intake to maintain body temperature to be normally constant. In addition, interleukin-lp, an endogenous pyrogen, enhanced turnover of neuronal histamine through prostaglandin E-2 in the brain. Taken together, the histamine neuron system in the hypothalamus is essential for maintenance of thermoregulation through the direct and indirect control of adaptive behavior. Behavioral and metabolic abnormalities of obese Zucker rats including hyperphagia, disruption of feeding circadian rhythm, hyperlipidemia, hyperinsulinemia, and disturbance of thermoregulation are essentially derived from a defect in hypothalamic neuronal histamine. Abnormalities produced by depletion of neuronal histamine from the hypothalamus in normal rats mimick those of obese Zuckers. Grafting the lean Zucker fetal hypothalamus into the obese Zucker pups attenuates those abnormalities. These findings indicate that histamine nerve systems in the brain play a crucial role in maintaining homeostatic energy balance. (C) Elsevier Science Inc. 1997.