在肥胖与非肥胖的多囊性卵巢综合征患者中补充失调
Alexandra E Butler1, Abu Saleh Md Moin1, Thozhukat Sathyapalan2
1Royal College of Surgeons in Ireland Bahrain, Busaiteen P.O. Box 15503, Adliya, Bahrain.
Cells
|August 11, 2023
概括
多囊性卵巢综合征 (PCOS) 涉及一种上调的替代补充通路,由肥胖加剧. 这种PCOS固有的特征在非肥胖和肥胖个体之间显示出不同的表型,观察到补体激活和抑制剂的增加.
科学领域:
- 免疫学 免疫学 免疫学
- 内分泌学 在内分泌学.
- 蛋白质组学是指蛋白质组学.
背景情况:
- 多囊卵巢综合征 (PCOS) 与补充系统因子上调有关,可能是由于肥胖和胰岛素抵抗.
- 这项研究调查了PCOS中补充因子的变化是固有的还是由代谢因素驱动的.
研究的目的:
- 为了比较肥胖和非肥胖的PCOS人群中的补充因子.
- 区分PCOS特异性补体变化与与肥胖和胰岛素抵抗相关的变化.
主要方法:
- 使用SOMA扫描技术进行等离子体蛋白质组分析.
- 在234名女性中测量了26种补充系统蛋白 (137名PCOS,97名对照).
- 对比肥胖/胰岛素耐药PCOS队列与非肥胖/非胰岛素耐药PCOS队列.
主要成果:
- 替代补充通路在肥胖和非肥胖的PCOS中都过度表达.
- 在两组中都观察到C3,properdin和因子I的增加;B因子在肥胖的PCOS中增加.
- 补充因子iC3b,C3d和C5a在PCOS两组都升高;C3a和C3adesArg在非肥胖PCOS中更高.
结论:
- 替代补充通路的上调是PCOS固有的,由肥胖恶化.
- 肥胖加剧了PCOS病理生理学,导致不同的非肥胖和肥胖的PCOS表型.
- 增加的补体激活被抑制剂抵消,这表明PCOS中对侮辱的反应被放大.
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