METABOLIC DYSFUNCTION AND INFLAMMATION IN CHILDHOOD SLEEP APNEA

儿童睡眠呼吸暂停中的代谢功能障碍和炎症

• 批准号: 7604578
• 负责人: ANN C HALBOWER
• 金额: $ 0.03万
• 依托单位: JOHNS HOPKINS UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-12-01 至 2007-09-16
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7604578
• 关键词: Adult; Apnea; Cardiovascular system; Child; Childhood; Computer Retrieval of Information on Scientific Projects Database; Dyslipidemias; Early Intervention; Fasting; Functional disorder; Funding; Grant; Hypertension; Hypoxemia; Inflammation; Inflammatory; Institution; Insulin; Insulin Resistance; Investigation; Leptin; Mediator of activation protein; Metabolic; Metabolic syndrome; Morbidity - disease rate; Obesity; Obstructive Sleep Apnea; Patients; Research; Research Personnel; Resources; Risk; Serum; Severities; Sleep Apnea Syndromes; Somatotropin; Source; United States National Institutes of Health; cardiovascular risk factor; cysteine rich protein; glucose tolerance; improved; mortality

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. The metabolic syndrome, (insulin resistance, dyslipidemia, hypertension, and obesity) is related to an increased risk for cardiovascular morbidity and mortality. An association between the metabolic syndrome and obstructive sleep apnea (OSA) has been found in adults. An increase in serum levels of inflammatory markers has also been previously documented in adult patients with OSA. Serum leptin and growth hormone, potential mediators of metabolic disturbances in sleep apnea, are increased by intermittent hypoxemia in adults with OSA. Apnea severity and hypoxemia appear to be independently predictive of glucose tolerance and insulin resistance. Little is known about the metabolic effects of sleep apnea in children. OSA correlates with serum levels of fasting insulin, leptin, and CRP levels in obese children, but the relationship of childhood sleep apnea and the metabolic syndrome independent of obesity is unknown. The association of childhood sleep apnea with the metabolic syndrome and inflammation requires investigation in order to determine if the cardiovascular risks associated with sleep apnea in adults are present in children. If sleep apnea is related to these risks, and if the metabolic syndrome is improved by sleep apnea treatment, early intervention may alter the morbidity of the cardiovascular consequences associated with sleep apnea in adults.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 代谢综合征（胰岛素抵抗、血脂异常、高血压和肥胖）与心血管发病率和死亡率的风险增加有关。 代谢综合征和阻塞性睡眠呼吸暂停（OSA）之间的关联已在成人中发现。 先前在患有OSA的成人患者中也记录了炎性标志物的血清水平的增加。 血清瘦素和生长激素，睡眠呼吸暂停代谢紊乱的潜在介质，增加了间歇性低氧血症的成人OSA。 呼吸暂停严重程度和低氧血症似乎是葡萄糖耐量和胰岛素抵抗的独立预测因素。关于儿童睡眠呼吸暂停的代谢影响知之甚少。在肥胖儿童中，OSA与血清空腹胰岛素、瘦素和CRP水平相关，但儿童睡眠呼吸暂停与代谢综合征的关系尚不清楚。 儿童睡眠呼吸暂停与代谢综合征和炎症的关系需要调查，以确定与成人睡眠呼吸暂停相关的心血管风险是否存在于儿童中。 如果睡眠呼吸暂停与这些风险有关，并且如果代谢综合征通过睡眠呼吸暂停治疗得到改善，则早期干预可能会改变成人中与睡眠呼吸暂停相关的心血管后果的发病率。