Role of hypothalamic neuropeptide Y neurons in the defective thermogenic response to acute cold exposure in fatty Zucker rats
Role of hypothalamic neuropeptide Y neurons in the defective thermogenic response to acute cold exposure in fatty Zucker rats
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DOI：
10.1016/s0306-4522(97)00121-8
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发表时间：
1997-09-01
期刊：
影响因子：
3.3
通讯作者：
Williams, G
中科院分区：
文献类型：
--
作者：
Bing, C;Pickavance, L;Williams, G
脂肪 Zucker 大鼠的产热能力受损，并且无法对寒冷暴露产生足够的产热反应，部分原因是棕色脂肪组织中产热的交感神经驱动力下降。神经肽 Y 在下丘脑弓状核神经元中合成并在室旁核中释放，刺激进食并抑制棕色脂肪组织活动。脂肪 Zucker 大鼠的神经肽 Y 神经元过度活跃，被认为会导致食欲亢进、能量消耗减少和肥胖。我们研究了脂肪和瘦 Zucker 大鼠中棕色脂肪组织的生热活性（以解偶联蛋白信使 RNA 水平测量）与下丘脑神经肽 Y 和神经肽 Y 信使 RNA 水平之间的关系，以响应寒冷暴露（4 摄氏度）2.5 和 18 小时。在瘦 Zucker 大鼠中，4°C 冷暴露 2.5 和 18 小时，解偶联蛋白信使 RNA 水平显着增加 3.5 倍（P
The fatty Zucker rat has impaired heat production and fails to mount an adequate thermogenic response to cold exposure, partly because of decreased sympathetic drive to thermogenesis in brown adipose tissue. Neuropeptide Y, synthesized in neurons of the hypothalamic arcuate nucleus and released in the paraventricular nucleus, stimulates feeding and inhibits brown adipose tissue activity. The neuropeptide Y neurons are overactive in fatty Zucker rats and are thought to contribute to hyperphagia, reduced energy expenditure and obesity. We have examined the relationship between thermogenic activity in brown adipose tissue (measured as uncoupling protein messenger RNA levels) and hypothalamic neuropeptide Y and neuropeptide Y messenger RNA levels in response to cold exposure (4 degrees C) for 2.5 and 18 h, in fatty and lean Zucker rats. In lean Zucker rats, cold exposure at 4 degrees C for 2.5 and 18 h significantly increased uncoupling protein messenger RNA levels by 3.5-fold (P