专变终端现场接线图:求助翻译高手!!

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The subsequent cloning of the Agrp gene58 identified a peptide, AGRP, with homology to agouti that is an antagonist of MC3 and MC4 receptors59. The demonstration that hypothalamic AGRP expression, like that of NPY and POMC, is localized to the arcuate nucleus58, and that it is upregulated by fasting60,61 and by leptin deficiency58, indicates that antagonism of CNS melanocortin receptors is important in body-weight regulation. Consistent with its role as an anabolic signalling molecule, AGRP causes hyperphagia when administered intracerebroventricularly (i.c.v.)62,63 or expressed transgenically59, and the increase of food intake following a single i.c.v.injectionofAGRPissustainedforuptoaweek62.AlthoughNPY is described as the most potent orexigenic molecule (that is, a molecule that stimulates increased energy intake) when the feeding response is measured over a few hours, its effects are short-lived in comparison to those of AGRP. AGRP must therefore be considered the most robust orexigenic molecule if potency is measured as the cumulative increment of energy intake after a single i.c.v. injection. The mechanism underlying the extraordinary duration of action of AGRP remains a fascinating area for further investigation.
Neuropeptide signalling pathways in the hypothalamus
Brainlesioningandstimulationstudiesperformedsomesixdecades ago first implicated the hypothalamus as a major centre controlling food intake and body weight (Fig. 3). As summarized in a classic paper by Stellar64, these studies identified the ventromedial hypothalamic nucleus (VMN) as the ‘satiety centre’, while the lateral hypothalamic area (LHA) was termed the ‘hunger centre’ (reviewed in ref. 50). These designations reflected the ability of electrical stimulation of the VMN to suppress food intake, and of bilateral VMN lesions to induce hyperphagia and obesity. Conversely, stimulation orlesioningoftheLHAinducedtheoppositesetofresponses.Asour knowledge of specific neuronal subpopulations involved in energy homeostasis has expanded, the notion of specific ‘centres’ of the brain that control food intake and body weight has been replaced by that of discrete neuronal pathways that generate integrated responses to afferent input related to changing body fuel stores65.

后来发现克隆的AgRPgene58胜、AGRP,homology,agouti,是对立的receptors59MC3和MC4. 示威,表达hypothalamicAGRP一样,POMC和NPY是局部的arcuatenucleus58,也是由upregulatedfasting60重男轻女,leptindeficiency58显示,通信、导航对抗melanocortin效很重要的体重量管制. 符合它作为一种类固醇信号分子,AGRP原因hyperphagia当管理intracerebroventricularly(I.C.V.)62,63或表达transgenically59、增加粮食摄入以下单一i.c.v.injectionofagrpissustainedforuptoaweek62.althoughnpy被视为最有力orexigenicDNA(即DNA是刺激更多能量摄入)当喂养反应测量了几个小时,其影响是短暂的比较与AgRP. AGRP必须考虑的最强劲orexigenic物质力量来衡量,如果因为累积的能量摄入量增加后一i.c.v. 注射. 根据这一机制的行动时间非常有趣AgRP地区仍作进一步调查. neuropeptide信号通路的甲状腺 brainlesioningandstimulationstudiesperformedsomesixdecades牵连的前第一丘脑作为主要食物摄入量与体重控制中心(附图3). 总结典型stellar64文件,研究确定了核心ventromedialhypothalamic(VMN)'satiety中心」,而横向hypothalamic区(LHA),称为「饥饿中心』(1139检讨. 50). 这些名称反映能力电疗的食物摄入VMN镇压,使两国VMNhyperphagia面积和肥胖. 反之,刺激orlesioningofthelhainducedtheoppositesetofresponses.asour了解具体分组神经参与能源homeo扩大的概念具体'中心'的大脑,控制饮食和体重已不复存在,取而代之的是,相关的神经通路,产生综合反应传入神经输入相关机构改变燃料stores65