劳斯莱斯和迈巴赫内饰: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:高考问答 时间:2024/05/01 15:41:30
Prominent among anabolic effector pathways is a circuit containing
neuropeptide Y (NPY). Injection of NPY into cerebral ventricles or directly into the hypothalamus of rats potently stimulates food intake38 and decreases energy expenditure while simultaneously inducing lipogenic enzymes in liver and white adipose tissue39. Consequently, continuous or repeated central administration of NPY leads readily to obesity38,40. Because NPY gene expression and secretion of the NPY peptide in the hypothalamus are increased during active depletion of body fat stores41,42 and/or reduced leptin/insulin signalling to the brain43, NPY meets the criteria for an anabolic signalling molecule. Moreover, leptin inhibits arcuate nucleus NPY gene expression44,45 and genetic knockout of NPY reduces hyperphagia and obesity in ob/ob mice46, indicating that the full response to leptin deficiency requires NPY signalling (Fig. 2a). The hyperphagic response to insulin-deficient diabetes is similarly accompanied by increased hypothalamic NPY synthesis and release47, and this response is blocked by insulin administration, either systemically or directly into the brain20. The finding that mice that lack NPY (but are otherwise genetically normal) have intact feeding responses, however, raises questions about the need for NPY when leptin or insulin levels are normal48. Alternatively, congenital absenceofamajorneuropeptidesuchasNPYmayelicitcompensatoryresponsesthatmasktheconsequencesofitsdeficiency,andfurther studyisrequiredtoresolvethisissue.Agouti-relatedprotein(AGRP), orexin (also known as ‘hypocretin’) and melanin-concentrating hormone (MCH) have subsequently been added to the list of candidate anabolic effector signalling molecules (Table 1).
Melanocortins suppress food intake
Candidatecataboliceffectorsignallingmoleculeshaveanoppositeset of characteristics. Melanocortins such as -melanocyte-stimulating hormone ( -MSH)49, as well as corticotropin-releasing hormone (CRH)50, thyrotropin-releasing hormone (TRH)51, cocaine- and are among a growing list of peptides that promote negative energy balance. Neuronal synthesis of these peptides increases in response to increased adiposity signalling in the brain. Among these, the melanocortin system stands out as being remarkable both for its complexityanditsimportancetoenergyhomeostasis.

肥胖的转导发信号入在第三脑室的地板附近位于的一个神经细胞的反应,弓形中坚力量是占领下丘脑的长度的大约一半神经细胞的池体的一件伸长(`弧象’)收藏品。NPYandAGRPareco-localizedinarcuatenucleusneurons60,61,显示出,一个唯一神经细胞的细胞类型可能包含多anaboliceffectormolecules。ThesubsequentfindingthatPOMCand推车在分明co地方化,但毗邻,弓形nucleusneurons66indicatesthatcircuitsoriginatinginthisbrainarea的子集高度专门了研究在能量同态的角色(。 4). 假说弓形中坚力量转换信息与发信号由leptin入一个神经细胞的反应有关由对leptin的地方microinjection的厌食反应支持入这area67和i.的无能。c.v. 减少摄食的leptin在弓形中坚力量以后是destroyed68,69。 大多数NPY/AGRP和POMC/CART神经元被找到了对coexpress leptin receptors16,17,并且神经元的两个类型是被调控的byleptin (asjudgedbychangesinneuropeptidegeneexpression),但以反对的方式。 因此, NPY/AGRP神经元由leptin, andconsequentlyareactivatedinconditionswhereleptinlevels禁止是low44,45,60,61。 虽然被学习的井,胰岛素缺乏也似乎激活这neurons20,47和胰岛素感受器官在弓形nucleus15高度被集中。 相反地,减少的胰岛素描绘的情况或leptin在弓形中坚力量禁止POMC70,71和CART52表示,并且这些激素的管理能防止或变稀这些neuropeptide反应。而且, involuntaryoverfeedinginrats, whichpotently禁止自发摄食,一旦体重增加了超过5%,得出POMC信使RNA水平增加三倍在弓形nucleus72。 示范厌食导致由leptin73或由不随意的overfeeding72由melanocortin感受器官反对者的集中管理扭转(在没有作用在摄食在对照动物)的低药量表明melanocortin发信号是增加的肥胖导致的厌食反应的斡旋人发信号对脑子。 采取一起,这些研究结果表明弓形中坚力量是一个主要站点为转换输入输入从流通的leptin和胰岛素入一个神经细胞的反应。

突出的在促合成动作器路之中是电路包含
neuropeptide Y (NPY)。 NPY的射入到大脑心室里或直接地到鼠里下丘脑有力地在肝脏和白色细胞脂肪tissue39时刺激食物intake38并且减少能量消耗,当同时导致lipogenic酵素。 结果, NPY的连续或重覆的集中管理欣然导致obesity38,40。 由于NPY NPY肽的基因表达和分泌物在下丘脑被增加在体脂肪期间stores41,42的活跃取尽并且/或者减少的leptin或者胰岛素发信号对brain43, NPY符合标准为一个促合成发信号的分子。 而且, leptin禁止弓形中坚力量NPY基因expression44,45,并且NPY基因击倒在ob/ob mice46减少hyperphagia和肥胖病,表明对leptin缺乏的充分的反应要求NPY发信号(。 2a)。 对胰岛素短少糖尿病的hyperphagic反应由增加的下丘脑NPY综合和release47相似地伴随,并且这个反应由胰岛素管理系统地阻拦,或者或直接地入brain20。 发现那缺乏NPY的老鼠(但是否则基因上法线)有原封哺养的反应,然而,关于需要的培养问题对NPY,当leptin或胰岛素水平是normal48时。 二者择一地,先天absenceofamajorneuropeptidesuchasNPYmayelicitcompensatoryresponsesthatmasktheconsequencesofitsdeficiency, andfurther studyisrequiredtoresolvethisissue。刺豚鼠relatedprotein (AGRP), orexin (亦称`hypocretin’)和黑色素集中激素(MCH)随后增加了到发信号分子(表1)的候选人促合成动作器名单。
Melanocortins压制摄食
特征Candidatecataboliceffectorsignallingmoleculeshaveanoppositeset。 Melanocortins例如-黑素细胞stimulating激素(- MSH) 49,并且corticotropin发布的激素(CRH) 50, thyrotropin发布激素(TRH) 51,可卡因和是在促进消极能量平衡肽的一张增长的名单之中。 这些肽神经细胞的综合增加以回应发信号在脑子的增加的肥胖。 在这些之中, melanocortin系统并肩作战象是卓越的两个为它的complexityanditsimportancetoenergyhomeostasis。