Central urocortin activation of sympathetic-regulated energy metabolism in Wistar rats

Central urocortin activation of sympathetic-regulated energy metabolism in Wistar rats
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DOI:
10.1016/s0006-8993(01)03401-1
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发表时间:
2002-03-15
期刊:
影响因子:
2.9
通讯作者:
Martínez, JA
Martínez, JA
中科院分区:
医学3区
文献类型:
--
作者:
De Fanti, BA;Martínez, JA

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促肾上腺皮质激素释放激素(CRH)系统包括促肾上腺皮质激素释放激素(CRH)和尿皮质激素(UCN),参与食欲和能量代谢的中枢控制。Urocortin是最近分离到的一种与CRH密切相关的神经肽,参与了抑制能量摄入的中枢信号级联反应,当Ucn在脑室和下丘脑内给药时,Ucn有效地减少了食物的摄入量。UCN受体虽然分布广泛,但在下丘脑核团中表达。由于下丘脑参与调节自主神经流出,UCN也可能作为一种分解代谢神经肽,通过交感神经调节的热再生促进能量消耗。为了验证UCN也通过激活交感神经系统来增加调节能量消耗的假设,我们检测了雄性Wistar大鼠在中枢给予UCN后的全身耗氧量(VO2)和结肠温度。也就是说,Wistar雄性大鼠(n=10)侧脑室注射1.0杯UCN,与PBS对照组相比,全身耗氧量显著增加。此外,与PBS组相比,UCN-组大鼠的结肠温度显著升高(Delta0.7+/-08℃),而神经节阻滞剂氯异丹明可阻止这一变化。这些研究表明,UCN通过中枢激活交感神经流出而显著增加全身耗氧量和体温。(C)2002 Elsevier Science B.V.保留所有权利。
The corticotropin-releasing hormone (CRH) system, including CRH and urocortin (UCN), is implicated in the central control of appetite and energy metabolism. Urocortin, a recently isolated neuropeptide closely related to CRH is involved in the central signaling cascade that inhibits energy intake, When administered intracerebroventricularly and intra-hypothalamically, UCN potently decreases food intake. Receptors for UCN, while widely distributed, are expressed in hypothalamic nuclei. As the hypothalamus is involved in modulating autonomic outflow, UCN may also act as a catabolic neuropeptide to facilitate energy expenditure through sympathetic-regulated thermoaenesis. To test the hypothesis that UCN also enhances regulatory energy expenditure via the activation of the sympathetic nervous system, we examined whole body oxygen consumption (VO2) and colonic temperature in male Wistar rats in response to central UCN administration. That is, the intracerebroventricular injection of 1.0 mug of UCN in male Wistar rats (n = 10) significantly increased whole body oxygen consumption compared to PBS control. In addition, colonic temperature was significantly increased (Delta0.7 +/-08 degreesC) in UCN- vs. PBS-administered rats, which was prevented by pretreatment with the ganglionic blocker chlorisondamine. These studies suggest that UCN acutely increased whole body oxygen consumption and body temperature via central activation of sympathetic outflow. (C) 2002 Elsevier Science B.V. All rights reserved.