MOREHOUSE CCRE DP1- ENDOTHELIAL FUNCTION IN OBESE AFRICAN AMERICAN WOMEN

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。 该项目的总体目标是探索炎症和氧化应激在肥胖的非裔美国女性中调节内皮功能的潜在作用。虽然肥胖和内皮功能受损之间的联系已经确立，但这种联系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，骨髓来源的内皮祖细胞参与血管修复。最近，心血管危险因素与循环内皮祖细胞数量减少、加速内皮祖细胞凋亡、血管形成能力受损和内皮功能障碍相关。这项研究的基础是肥胖代表了血管病理的临床前状态，因此，它是一个独特的模型，可以用来探讨这些内皮祖细胞在肥胖血管内皮功能损害中的作用。认识到决定内皮最终状态的生理相互作用的复杂性，我们建议探索肥胖与内皮关系的机制基础 通过结合饮食干预来发挥作用，饮食干预包含一种已知的营养成分，它可以增强抗氧化能力，同时提供有利的血脂和葡萄糖耐量。从长远来看，这应该会提高我们对肥胖与血管疾病关系的基础的理解，并可能有助于为这些高危人群设计饮食干预措施。

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 marrowderived 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.