血管内皮功能障碍（Endothelial dysfunction）在肥胖儿童早期动脉粥样硬化形成中起关键作用，并促进其成年后心血管疾病发生。目前已知规律运动可改善肥胖儿童血管内皮功能，降低其代谢综合征、心血管疾病发病风险。但有关改善肥胖儿童血管内皮功能障碍的有效运动干预措施及分子生物学机制尚未明确。本项目拟选择单纯性肥胖儿童为研究对象，观察不同形式运动干预对其血管内皮功能障碍及生化标记物的影响，并通过高脂膳食建立肥胖大鼠模型，采用相关分子生物学及形态学技术研究不同形式运动干预后其脂肪组织肾素-血管紧张素系统（RAS）活性成分、血管内皮细胞AngⅡ及胰岛素信号转导相关蛋白表达及形态学改变，阐明不同形式运动干预对肥胖儿童血管内皮功能的影响及机制。本项目的实施对深入了解运动干预改善肥胖儿童血管内皮功能障碍，预防代谢综合征及心血管疾病的分子机制具有重要意义，同时为优化肥胖儿童运动处方提供科学依据。

Endothelial dysfunction plays a key role in the early formation of atherosclerosis in obese children, and promotes the occurrence of adult cardiovascular disease. At present, regular exercise can improve endothelial function in obese children, and reducing the metabolic syndrome and cardiovascular disease risk has been recognized. But the effective measures about exercise improving the vascular endothelial dysfunction in obese children and its molecular mechanism is not yet clear. This project tests the effects of different exercise intervention on vascular endothelial dysfunction and its biochemical markers, and investigates effects and mechanisms of different exercise intervention on the vascular endothelial function in obese children by means of check RAS in adipose tissue, expression of Ang II and insulin signaling cascade associated proteins in endothelial cell, cell morphological changes with molecular biology and morphology techniques to high fat diet-induced obese rat. The implementation of this project has vital significance to understand molecular mechanisms about exercise prevent metabolic syndrome and cardiovascular disease through improve endothelial dysfunction in obese children; thereby provide scientific basis for optimization of exercise prescription in obese children.