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首页> 外文期刊>The European Journal of Neuroscience >Effects of albumin-conjugated PYY on food intake: the respective roles of the circumventricular organs and vagus nerve
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Effects of albumin-conjugated PYY on food intake: the respective roles of the circumventricular organs and vagus nerve

机译：白蛋白缀合的PYY对食物摄入的影响：室室器官和迷走神经的各自作用

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摘要

The mechanism and routes through which peptide tyrosine-tyrosine (PYY) exerts its anorectic effects are still largely unknown. In the present study, we investigated the roles of the area postrema (AP), subfornical organ (SFO) and vagus nerve in mediating the anorectic effect of PYY using PYY_(3-36) conjugated to human serum albumin (PYY_(3-36)-HSA) in rats. PYY_(3-36)-HSA is a large molecule that does not penetrate the blood-brain barrier, and thus provides a useful tool to discriminate between the central (brain) and peripheral actions of this peptide. PYY_(3-36)-HSA induced significant reductions in food and body weight gain up to 24 h after administration. The anorectic effect of PYY_(3-36)-HSA was delayed for 2 h in rats in which both AP and SFO were ablated, while lesion of either of these circumventricular organs in isolation did not influence the feeding responses to PYY_(3-36)-HSA. The PYY_(3-36)-HSA-induced anorectic effect was also reduced during the 3- to 6-h period following subdiaphragmatic vagotomy. Lesions of AP, SFO and AP/SFO as well as subdiaphragmatic vagotomy blunted PYY_(3-36)-HSA-induced expression of c-fos mRNA in specific brain structures including the bed nucleus of stria terminalis, central amygdala, lateral-external parabrachial nucleus and medial nucleus of the solitary tract. In addition, subdiaphragmatic vagotomy inhibited the neuronal activation induced by PYY_(3-36)-HSA in AP and SFO. These findings suggest that the anorectic effect and brain neuronal activation induced by PYY_(3-36)-HSA are dependent on integrity of AP, SFO and subdiaphragmatic vagus nerve.
机译：肽酪氨酸-酪氨酸（PYY）发挥其厌食作用的机制和途径仍是未知之数。在本研究中，我们研究了人后白蛋白（PYY_（3-36）与人血清白蛋白（PYY_（3-36） ）-HSA）。 PYY_（3-36）-HSA是不会穿透血脑屏障的大分子，因此提供了一种有用的工具来区分该肽的中枢（脑）和外周作用。 PYY_（3-36）-HSA可以在给药后24小时内显着降低食物和体重增加。消融AP和SFO的大鼠PYY_（3-36）-HSA的厌食作用延迟了2小时，而孤立的这两个脑室器官的病变并不影响对PYY_（3-36）的摄食反应）-HSA。 PYY_（3-36）-HSA诱导的厌食作用在dia下迷走神经切断术后3至6小时内也有所降低。 AP，SFO和AP / SFO的病变以及dia肌迷走神经切断术使PYY_（3-36）-HSA诱导的c-fos mRNA在特定大脑结构中表达，包括终末纹状体床核，杏仁核中央，外侧臂外侧副臂核和孤立道的内侧核。此外，dia下迷走神经切断术抑制了PYY_（3-36）-HSA在AP和SFO中诱导的神经元活化。这些发现表明，PYY_（3-36）-HSA引起的厌食作用和脑神经元激活取决于AP，SFO和dia下迷走神经的完整性。

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