DIVA

歌姬

• 批准号: 7609634
• 负责人: PRISCILLA E PEMU
• 金额: $ 7.18万
• 依托单位: MOREHOUSE SCHOOL OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-08-01 至 2008-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7609634
• 关键词: African American; Antioxidants; Apoptosis; Blood Vessels; Bone Marrow; Computer Retrieval of Information on Scientific Projects Database; Diet; Dietary Intervention; Endothelium; Funding; Grant; Impairment; Individual; Inflammation; Institution; Intervention; Lipids; Modeling; Numbers; Nutrient; Obesity; Oxidative Stress; Pathology; Personal Satisfaction; Physiological; Regenerative Medicine; Research; Research Personnel; Resources; Risk; Role; Source; Stem cells; United States National Institutes of Health; Vascular Diseases; Woman; base; cardiovascular risk factor; design; glucose tolerance; improved; pre-clinical; repaired

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 overall objective of this project is to explore the potential role of inflammation and oxidative stress in modulating endothelial function among obese African American women. Although the association between obesity and impaired endothelial function is well established, the exact mechanism of this association remains unclear. We will examine the impact of obesity-related inflammation and oxidative stress on circulating levels of endothelial progenitor cells. Exciting new research in regenerative medicine has identified bone marrow-derived endothelial progenitor cells that are involved in vessel repair. Most recently, cardiovascular risk factors have been correlated with decreased numbers of circulating endothelial progenitor cells (EPCs), accelerated EPC apoptosis, impairment of vessel forming capacity and endothelial dysfunction.The proposed study relies on the fact that obesity represents a pre-clinical state of vascular pathology; therefore, it is a unique model that can be used to explore the role of these EPCs in the impairment of endothelial function of obesity. Recognizing the complexity of physiological interactions that determine the ultimate state of the endothelium, we propose to probe the mechanistic basis of the relationships between obesity and endothelial function by incorporating a diet intervention which comprises a nutrient composition that is known to augment antioxidant capacity while providing favorable lipid profiles and glucose tolerance. Long- term, this should improve our understanding of the basis for the relationship of obesity to vascular disease and may help in the design of dietary interventions in these high-risk individuals.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 该项目的总体目标是探索炎症和氧化应激在调节肥胖非裔美国女性内皮功能中的潜在作用。尽管肥胖与内皮功能受损之间的关联已得到充分证实，但这种关联的确切机制仍不清楚。我们将研究肥胖相关炎症和氧化应激对内皮祖细胞循环水平的影响。再生医学领域令人兴奋的新研究发现了参与血管修复的骨髓来源的内皮祖细胞。最近，心血管危险因素与循环内皮祖细胞 (EPC) 数量减少、EPC 细胞凋亡加速、血管形成能力受损和内皮功能障碍相关。这项研究基于肥胖代表临床前状态的事实。血管病理学；因此，它是一个独特的模型，可用于探索这些EPCs在肥胖引起的内皮功能损伤中的作用。 认识到决定内皮细胞最终状态的生理相互作用的复杂性，我们建议通过纳入饮食干预来探讨肥胖与内皮功能之间关系的机制基础，该饮食干预包含已知可增强抗氧化能力同时提供有利的营养成分。血脂和葡萄糖耐量。从长远来看，这应该会提高我们对肥胖与血管疾病关系基础的理解，并可能有助于设计这些高危人群的饮食干预措施。