氧化抵抗与胰岛素耐药肥胖儿童的血管和心肌功能障碍有关:一项新型大动脉应变研究
Antoine Fakhry AbdelMassih1,2, Fatma Alzahraa Mostafa1, Marianne Edward Yassa3
1Department of Pediatrics, Pediatric Cardiology Unit, Cairo University Children Hospital, Cairo University, Cairo, Egypt.
Journal of cardiovascular echography
|September 15, 2025
概括
肥胖导致较高的氧化 (NOx) 水平,这表明胰岛素抵抗会影响NO的生物可用性. 这种与大动脉应变率相关的血管功能障碍会影响心肌功能,特别是在心下内脏.
科学领域:
- 心血管生理学心血管生理学
- 代谢障碍 代谢障碍 代谢障碍
- 生物化学 生物化学
背景情况:
- 已知肥胖会损害血管顺应性和心肌功能.
- 肥胖引起的心血管功能障碍背后的确切机制尚不清楚.
- 关于肥胖中氧化 (NOx) 调节的证据存在矛盾.
研究的目的:
- 为了研究肥胖个体的NOx状态.
- 为了将NOx水平与血管功能参数相关联.
- 确定在肥胖中血管功能障碍和心肌功能之间的关系.
主要方法:
- 招募了20名肥胖患者和16名健康对照.
- 测量了血清NOx水平和食后C-与葡萄糖比率 (PCPRI).
- 使用流媒扩张 (FMD) 和大动脉应变率 (ASR) 评估了血管功能.
- 用斑点跟踪回声心脏成像来评估心肌功能.
主要成果:
- 肥胖患者的血清NOx明显高 (106 ± 14) 与对照组 (62 ± 9) 相比.
- 增加的PCPRI (表明胰岛素耐药性) 与更高的NOx水平相关,这表明胰岛素诱导的NOx耐药性.
- ASR与血清NOx (r=0.86) 呈现出强烈的相关性,比口疫 (r=0.66) 更强烈.
- 降低ASR与心肌功能受损有关,特别是心下内脏的全球纵向应变 (r=0.77).
结论:
- 肥胖相关的血管功能障碍可能源于高胰岛素血症诱导的氧化耐药性.
- 这种血管功能障碍似乎显著降低了心肌功能,特别是由于血液供应受损害,影响心下内脏区域.
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