MOREHOUSE CCRE DP1- ENDOTHELIAL FUNCTION IN OBESE AFRICAN AMERICAN WOMEN

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。 该项目的总体目标是探讨炎症和氧化应激在调节肥胖的非裔美国妇女的内皮功能中的潜在作用。虽然肥胖和内皮功能受损之间的关联已经得到了很好的证实，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循环内皮祖细胞水平的影响。令人兴奋的再生医学新研究已经确定了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（EPC）数量减少，加速EPC凋亡，血管形成能力受损和内皮功能障碍有关。该研究基于肥胖代表血管病理学的临床前状态，因此，它是一种独特的模型，可用于探索这些EPCs在肥胖内皮功能受损中的作用。认识到决定内皮最终状态的生理相互作用的复杂性，我们建议探索肥胖和内皮细胞之间关系的机制基础。 通过结合饮食干预来发挥作用，所述饮食干预包括已知增加抗氧化能力同时提供有利的脂质分布和葡萄糖耐受性的营养组合物。从长远来看，这将提高我们对肥胖与血管疾病关系的基础的理解，并可能有助于设计这些高危人群的饮食干预措施。

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.