CONTROL OF GONADOTROPIN SECRETION DURING LACTATION

哺乳期间促性腺激素分泌的控制

• 批准号: 8173173
• 负责人: M. SUSAN SMITH
• 金额: $ 15.22万
• 依托单位: OREGON HEALTH & SCIENCE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-05-01 至 2011-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8173173
• 关键词: Amenorrhea; Anorexia Nervosa; Computer Retrieval of Information on Scientific Projects Database; Controlled Study; Eating; Exercise; Funding; Gonadotropin Hormone Releasing Hormone; Gonadotropins; Grant; Hyperphagia; Hypothalamic structure; Institution; Insulin; Lactation; Leptin; Macaca mulatta; Malnutrition; Milk; Neurons; Neuropeptides; Periodicity; Physiological; Production; Research; Research Personnel; Resources; Signal Transduction; Source; Study models; System; Techniques; United States National Institutes of Health; Woman; base; energy balance; hypocretin; inhibitory neuron; melanin-concentrating hormone; relating to nervous system; reproductive; reproductive function

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Lactation is characterized by an inhibition of reproductive cyclicity due to a suppression of gonadotropin releasing hormone (GnRH), excessive hyperphagia and negative energy balance due to milk production. The central hypothesis of this proposal is that suppression of GnRH/LH secretion is due to suckling-induced alterations in hypothalamic neural systems that regulate food intake and energy balance. Our studies have recently established that several hypothalamic neuropeptide orexigenic systems involved in regulating food intake/energy balance (NPY, orexin, melanin concentrating hormone) make direct connections with GnRH neurons, thus providing a neuroanatomical framework by which signals denoting changes in food intake/energy balance can be directly transmitted to GnRH neurons. Using electrophysiological techniques, we showed that NPY has direct inhibitory effects on GnRH neurons; these inhibitory effects are greatly increased during lactation. If the suppressed levels of leptin and/or insulin were restored to normal postlactation levels , there is no effect on the hyperphagia or the suppressed LH secretion during lactation. These results suggest that the negative energy balance of lactation is not a prerequisite for the hyperphagia or the suppression of GnRH/LH. The interaction between reproductive function and energy balance during lactation provides a physiological model for studying a number of conditions in women (undernutrition, anorexia nervosa, bulimia and exercise-induced amenorrhea) that involve a suppression of reproductive function associated with changes in energy balance. The results of the studies formed the basis of a new funded project to study control of food intake in the rhesus monkey.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 哺乳化的特征是由于促性腺激素释放激素（GNRH），过度镀膜和由于牛奶产生而导致的负能量平衡，抑制了生殖环节性。该提案的中心假设是，抑制GnRH/LH分泌是由于哺乳诱导的下丘脑神经系统的改变引起的调节食物摄入量和能量平衡的改变。我们的研究最近确定，几种参与调节食物摄入/能量平衡（NPY，OREXIN，黑色素浓缩激素）的下丘脑神经肽的原始系统与GNRH神经元建立了直接连接，从而可以通过表达对食物进型/能量平衡的指示性的变化可以使神经融合框架直接跨性别transins transs transits transits transins transmits gn。使用电生理技术，我们表明NPY对GNRH神经元具有直接的抑制作用。这些抑制作用在泌乳过程中大大增加。 如果将抑制水平的瘦素和/或胰岛素恢复到正常的后乳液水平，则对哺乳期的肉质或抑制的LH分泌没有影响。 这些结果表明，泌乳的负能量平衡不是噬菌体或抑制GnRH/LH的先决条件。泌乳期间生殖功能与能量平衡之间的相互作用为研究女性的多种疾病（营养不良，神经性厌食症，贪食症和运动诱导的闭经）提供了生理模型，涉及抑制与能量平衡变化相关的生殖功能。研究结果构成了一个新资助的项目的基础，以研究恒河猴中食物摄入的控制。