中科新闻网p3下位村关键任务:求助翻译高手!!
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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.
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.
突出的在促合成动作器路之中是包含neuropeptide Y (NPY)的电路。 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的活跃取尽和或减少的leptin/发信号对brain43的胰岛素， 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/减少hyperphagia和肥胖病ob mice46， 表明对leptin缺乏的充分的反应要求NPY发信号(。 2a)~~~~~~~~~~~~剩下的你自己解决吧~~~~连一点点悬赏分也不给~~~解决问题~~???!!!!