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急性冷暴露大鼠下丘脑局部神经肽Y水平普遍升高。

Widespread increases in regional hypothalamic neuropeptide Y levels in acute cold-exposed rats.

作者信息

McCarthy H D, Kilpatrick A P, Trayhurn P, Williams G

机构信息

Department of Medicine, University of Liverpool, U.K.

出版信息

Neuroscience. 1993 May;54(1):127-32. doi: 10.1016/0306-4522(93)90388-v.

DOI:10.1016/0306-4522(93)90388-v
PMID:8515838
Abstract

Neuropeptide Y injected into the hypothalamus or third ventricle stimulates feeding and inhibits the sympathetic activation of brown adipose tissue. To clarify the involvement of hypothalamic neuropeptide Y in cold-induced thermogenesis, groups of rats exposed to 4 degrees for 2.5 or 18 h were compared with warm-adapted rats (22 degrees C). Neuropeptide Y was measured in eight selected hypothalamic regions, including those known to be involved in the regulation of energy expenditure. Activation of brown adipose tissue was confirmed by significant six- to nine-fold increases in brown adipose tissue uncoupling protein messenger RNA. Compared with warm-adapted controls, neuropeptide Y levels were significantly raised by 80-170% in several hypothalamic regions of rats exposed to cold for 2.5 h, namely the medial preoptic area, paraventricular nucleus, ventromedial nucleus, dorsomedial nucleus and lateral hypothalamic area. Neuropeptide Y levels in 18-h cold-exposed rats were similarly elevated in these regions and were also significantly increased in the anterior hypothalamic area (75%). By contrast, neuropeptide Y levels in the arcuate nucleus, the main hypothalamic site of synthesis, were not increased by cold exposure, being significantly reduced by 21% after 2.5 h exposure and comparable with controls after 18 h. As neuropeptide Y injection inhibits brown adipose tissue activation, we suggest that the rapid and dramatic increases in neuropeptide Y levels in specific hypothalamic regions occur because cold exposure might inhibit the release of neuropeptide Y and so cause accumulation of neuropeptide Y in these sites.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

注入下丘脑或第三脑室的神经肽Y会刺激进食,并抑制棕色脂肪组织的交感神经激活。为了阐明下丘脑神经肽Y在冷诱导产热中的作用,将暴露于4摄氏度环境2.5小时或18小时的大鼠组与适应温暖环境(22摄氏度)的大鼠进行比较。在八个选定的下丘脑区域测量神经肽Y,包括那些已知参与能量消耗调节的区域。棕色脂肪组织解偶联蛋白信使核糖核酸显著增加6至9倍,证实了棕色脂肪组织的激活。与适应温暖环境的对照组相比,暴露于寒冷环境2.5小时的大鼠的几个下丘脑区域,即视前内侧区、室旁核、腹内侧核、背内侧核和下丘脑外侧区的神经肽Y水平显著升高80 - 170%。在这些区域,暴露于寒冷环境18小时的大鼠的神经肽Y水平同样升高,并且在下丘脑前部区域也显著增加(75%)。相比之下,合成神经肽Y的主要下丘脑部位弓状核中的神经肽Y水平并未因寒冷暴露而增加,暴露2.5小时后显著降低21%,18小时后与对照组相当。由于注射神经肽Y会抑制棕色脂肪组织的激活,我们认为特定下丘脑区域中神经肽Y水平的快速显著升高是因为寒冷暴露可能抑制了神经肽Y的释放,从而导致神经肽Y在这些部位积累。(摘要截断于250字)

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