NEUROHORMONAL REGULATION OF ENERGY BALANCE AMONG PEDIATRIC BRAIN TUMOR SUBJECTS

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 某些类型的儿童脑瘤的幸存者患病态肥胖的风险很大。这种机制被认为在很大程度上是由于下丘脑对摄食的调节失调。虽然已经确定了许多调节摄食的神经激素信号通路，但没有一条是在最有肥胖风险的神经肿瘤学受试者中进行专门评估的。考虑到这些受试者中的许多人在手术前具有正常的能量平衡，然后在手术后迅速下降，观察神经激素信号的纵向变化的观察性研究可以进一步阐明这些患者肥胖的潜在机制，并提供对肥胖的一般激素调节的洞察。 在这项先导研究中，我们将前瞻性地评估新诊断的儿童原发性脑肿瘤患者，并比较那些与体重增加相关的肿瘤(间脑肿瘤)和那些与体重增加无关的肿瘤。具体地说，我们将评估神经激素浓度的变化，监测饮食和锻炼作为体重增加的工具，并评估可能导致能量平衡失调的潜在内分泌功能障碍。随着对肥胖潜在的神经激素生理学有了更好的了解，最终可以确定这一具有挑战性的并发症的潜在治疗目标。

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. Survivors of certain types of pediatric brain tumors are at significant risk for developing morbid obesity. The mechanism is thought to be largely due to hypothalamic dysregulation of feeding. While many of the neurohormonal signaling pathways for the regulation of feeding have been identified, none have been evaluated specifically in the neuro-oncology subjects most at risk for obesity. Given that many of these subjects pre-operatively have normal energy balance and then rapidly decline post-operatively, an observational study looking at the longitudinal changes in neurohormonal signals could further elucidate the underlying mechanisms for obesity in these patients, as well as providing insight into the hormonal regulation of obesity in general. In this pilot study, we will prospectively evaluate newly diagnosed subjects with primary pediatric brain tumors and compare those with tumors associated with weight gain (diencephalic tumors) to those with tumors not associated with weight gain. Specifically, we will evaluate changes in neurohormone concentrations, monitor diet and exercise as the vehicle for weight gain, and assess underlying endocrine dysfunction that may contribute to energy balance dysregulation. With a better understanding of the underlying neurohormonal physiology of obesity, potential therapeutic targets for this challenging complication can ultimately be identified.