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: BAYLOR COLLEGE OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-12-01 至 2006-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7375001
• 关键词: INSULIN; RESISTANCE; CYTOKINES; BONE; MINERAL

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.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。患有囊性纤维化（CF）的儿童经常会出现反复的肺部感染，使他们暴露于慢性炎症。这种炎症可能导致外周胰岛素抵抗，葡萄糖代谢恶化，导致一些人患上糖尿病。过去的研究已经证实了胰岛素缺乏症，但关于胰岛素抵抗作为囊性纤维化相关糖尿病（CFRD）的一个因素的结果相互矛盾。炎症标志物也与骨分解增加有关，这可能在该人群的骨质疏松症中发挥作用。本研究的目的是调查CF儿童，特别是观察血清炎症介质，胰岛素抵抗和骨密度，以及它们之间可能的相互作用。这一领域的大多数CF研究都是在年轻的成年患者中进行的。很少有人研究年轻的CF人群，特别是那些不到6岁的。在如此年轻的时候认识到胰岛素抵抗和骨密度降低可能会导致针对这些领域的早期干预的治疗。通过改善葡萄糖代谢，这些儿童将获得更好的营养状态，使他们更强壮地对抗感染，或减少感染的数量，抑制感染导致炎症的恶性循环，从而导致营养恶化和骨分解增加。研究表明，当葡萄糖代谢正常化时，成人CF人群的肺功能改善。我们希望，这些改善将导致提高这一人口的生活质量和预期寿命。