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INSULIN RESISTANCE, CYTOKINES AND BONE MINERAL DENSITY IN CHILDREN WITH CYSTI

INSULIN RESISTANCE, CYTOKINES AND BONE MINERAL DENSITY IN CHILDREN WITH CYSTI
患有 Cysti 的儿童的胰岛素抵抗、细胞因子和骨矿物质密度
批准号:
7375001
负责人:
MOREY W HAYMOND
金额:
$4.99万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2005
资助国家:
美国
项目状态:
已结题
起止时间:
2005-12-01 至 2006-11-30

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中文摘要
翻译
本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者(PI)可能已经从另一个NIH来源获得了主要资金,因此可以在其他CRISP条目中表示。列出的机构是中心的,不一定是研究者的机构。患有囊性纤维化(CF)的儿童经常发生复发性肺部感染,使他们暴露于慢性炎症。这种炎症可导致外周胰岛素抵抗,使葡萄糖代谢恶化,导致部分人患上糖尿病。过去的研究证实了胰岛素缺乏,但胰岛素抵抗作为囊性纤维化相关性糖尿病(CFRD)的一个因素显示了相互矛盾的结果。炎症标志物也与骨质破坏增加有关,这可能在该人群的骨质疏松症中起作用。本研究的目的是调查CF患儿,特别关注血清炎症介质、胰岛素抵抗和骨密度,以及它们之间可能的相互作用。该领域的大多数CF研究都是针对年轻成年期的患者。很少有人研究年轻的CF人群,特别是6岁以下的CF人群。在如此年轻的年龄就认识到胰岛素抵抗和骨密度下降可能导致针对这些领域的早期干预治疗。通过改善葡萄糖代谢,这些孩子将有更好的营养状态,使他们更强壮地抵抗感染,或减少感染的数量,抑制感染导致炎症、营养恶化和骨质破坏的恶性循环。研究表明,当糖代谢正常化后,成年CF患者的肺功能得到改善。我们希望这些改进将改善这一人群的生活质量,延长预期寿命。
英文摘要
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. Children with Cystic Fibrosis (CF) often develop recurrent pulmonary infections, exposing them to chronic inflammation. This inflammation may lead to peripheral insulin resistance, worsening glucose metabolism, leading to frank diabetes in some. Past studies have confirmed insulinopenia, but have shown conflicting results concerning insulin resistance as a factor in Cystic Fibrosis Related Diabetes (CFRD). Inflammatory markers have also been associated with increased bone breakdown, which may play a role in osteoporosis in this population. The purpose of this study is to investigate children with CF, looking specifically at serum inflammatory mediators, insulin resistance and bone density, and the possible interplay between them. Most of the CF studies in this area have been in patients in young adulthood. Few have studied the young CF population, especially those less than 6 years of age. The recognition of insulin resistance and decreased bone density at such a young age may lead to therapies targeting earlier intervention in these areas. By improving glucose metabolism, these children will have better nutritional states which make them stronger to fight off infections, or reduce the amount of infections they acquire, inhibiting the vicious cycle of infection leading to inflammation leading to worsened nutrition and increased bone breakdown. Studies have shown improved lung function in the adult CF population when glucose metabolism has been normalized. We are hopeful that these improvements will lead to improved quality of life and increased life expectancy in this population.
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