三亚十大婚纱品牌:翻译(有分吆,翻译的好还加分呢???!!我有的是分)

来源:百度文库 编辑:高校问答 时间:2024/04/28 17:56:24
Evidence that MCH synthesis is elevated by both energy restriction and leptin deficiency79,andthatMCH-knockoutmicehavereducedfoodintake andareexcessivelylean80,isconsistentwiththismodel.Thediscovery of the MCH receptor as a G-protein-coupled receptor (previously knownasSLC-1)81,82alsosupportsthehypothesisofMCHasanorexigenicfactor.LikeNPYreceptors,theMCHreceptoriscoupledtothe Gi subunit of the plasma membrane G-protein assembly. By activating Gi, binding of MCH to its receptor inhibits formation of cyclic

AMP and consequently reduces signalling by protein kinase A (PKA)81,82. This effect is opposite to that mediated by activation of receptors that exert anorexic effects, such as MC4 or CRH receptors, which are coupled to Gs and consequently increase cAMP and PKA signalling. Two additional peptides are expressed exclusively in the LHA, zona incerta and PFA. Termed ‘hypocretins 1 and 2’83 or ‘orexins A and B’84 by the two groups that simultaneously discovered them, these peptides increase food intake and cause generalized behavioural arousal when administered centrally84,85. Targeted deletion of the hypocretin/orexin gene in mice induces narcolepsy86, a disorder characterized by the sudden onset of sleep at times when it would not ordinarily occur. This finding indicates that reduced hypocretin/orexinsignallingmaycontributetotheonsetandmaintenanceof sleep, in addition to its potential role in the control of food intake. Integration of MCH and hypocretin/orexin neurons into a model of the hypothalamic pathways controlling energy homeostasis predicts that they should be inhibited by melanocortin or CART input, and stimulated by NPY signalling, from neurons of the arcuate nucleus. Much work must be done to test this model of first- and secondorder neurons in the energy homeostasis circuit. Identifying specific neuronal subsets in the PVN and LHA that express NPY and melanocortin receptors is an important priority. Because many neurons of the PVN, PFA and LHA project to the arcuate nucleus, neuronal traffic flows bidirectionally between the arcuate nucleus and these other hypothalamic sites. So rather than being passive recipients of information from the arcuate nucleus, these secondorder neurons can actively modify the information that arrives there. In addition, leptin receptors have been described on PVN and LHA neurons,implicatingthemasdirecttargetsforregulationbycirculating adiposity signals.

藉着能源限制和 leptin 缺乏 79 , MCH 综合是提高的证据,andthatMCH-knockoutmicehavereducedfoodintake 的 andareexcessivelylean 80 , isconsistentwiththismodel。如 a G 的 MCH 受容器的 Thediscovery-蛋白质加倍的受容器 (先前 knownasSLC-1)81,82alsosupportsthehypothesisofMCHasanorexigenicfactor.LikeNPYreceptors,血浆薄膜 G-蛋白质的集会 theMCHreceptoriscoupledtothe Gi 次单位。 藉由启动 Gi, 对它的受容器的 MCH 的绑禁止循环的形成

安培和结果藉着蛋白质 kinase 一 (PKA)81,82 减少作信号.这效果是相对事物对那藉着发挥 anorexic 效果, 像是 MC4 或者 CRH 受容器的受容器的使活动斡旋了, 这被加倍到 Gs 而且结果增加露营和 PKA 作信号。 二个另外的缩氨酸在 LHA , zona incerta 和 PFA 中被独有地表达。 称了同时地发现了他们的二个团体的 'hypocretins 1 和 21983 或者 ' orexins 一和 B'84,当在中心管理了 84,85 ,这些缩氨酸增加食物摄取,而且因素推广了行为的觉醒。在老鼠中对准 hypocretin/orexin 基因的划除引诱它不通常发生的嗜眠发作 86 ,有时有睡眠的突然攻击的特点的混乱。除了食物摄取的控制的它的潜在角色之外,这一个发现指出 , 那减少了 hypocretin/orexinsignallingmaycontributetotheonsetandmaintenanceof 睡眠。 进入控制能源体内平衡的丘脑下部路的一个模型之内的 MCH 和 hypocretin/orexin 神经原的整合预测他们应该被 melanocortin 或手推车输入禁止而且被向 NPY 作信号的刺激,从 arcuate 核心的神经原。 很多的工作一定被做测试第一的这一个模型- 和能源体内平衡线路的 secondorder 神经原。 在 PVN 和明确的 NPY 和 melanocortin 受容器是重要的优先的 LHA 中识别特定的 neuronal 子集。因为 PVN, PFA 和 LHA 的许多神经原对 arcuate 核心计画,neuronal 交通双向性在 arcuate 核心和这些其他的丘脑下部的位置之间流动。 因此不愿身为来自 arcuate 核心的数据的消极接受者 , 这些 secondorder 神经原能积极地修正在那里到达的数据。 除此之外, leptin 受容器已经在 PVN 和 LHA 神经原, implicatingthemasdirecttargetsforregulationbycirculating 脂肪过多信号上被描述。