葡萄糖不耐受是由于肥胖小鼠后代的造血干细胞功能障碍造成的
Merve Denizli1, James Ropa2, Lindsay Beasley3
1Department of Pediatrics, Neonatal-Perinatal Medicine, Indiana University School of Medicine, Indianapolis, 46202, USA.
Molecular metabolism
|August 14, 2024
概括
孕产妇肥胖会根据性别不同地影响后代的造血干细胞和原生细胞 (HSPC). 肥胖母亲的男性后代表现出HSPC功能受损和葡萄糖不耐受,突出了性别特异性的对代谢健康的影响.
科学领域:
- 生殖生物学 生殖生物学
- 发育生物学是发展生物学.
- 代谢健康 代谢健康
背景情况:
- 孕产妇肥胖是一个越来越令人担忧的问题,增加后代的风险与造血和代谢系统相关的疾病.
- 后代的性别影响疾病易感性,这表明母亲的肥胖可能会导致血造干细胞和原生细胞 (HSPC) 功能的性别特异性变化.
- 孕产妇肥胖对后代HSPC功能及其在代谢调节中的作用的确切影响仍然不清楚.
研究的目的:
- 调查母亲肥胖对后代的性别特异性影响HSPC功能.
- 确定肥胖母亲后代的HSPC功能变化是否会导致代谢功能障碍.
- 测试孕产妇肥胖导致后代的性别依赖性重编程HSPC影响代谢健康的假设.
主要方法:
- 在出生以控制和饮食诱导的肥胖母鼠中评估HSPC表型,分别在出生后的第21天和第8周.
- 使用从P21小鼠中分类的HSPC进行了竞争性初级和二级移植.
- 在移植受体中对HSPC和代谢评估 (葡萄糖和胰岛素耐受性测试) 进行了转录基因分析 (RNA-seq).
主要成果:
- 与对照组相比,来自肥胖的男性后代的HSPC数量减少,植入能力受损.
- 肥胖母的雌性后代在很大程度上表现出不受影响的HSPC数量和功能,RNA-seq表明免疫刺激途径.
- 从肥胖母亲的男性后代中移植HSPC的接受者发展出葡萄糖不耐受性,而从女性后代中接受HSPC的接受者没有.
结论:
- 孕产妇的肥胖暴露对后代的HSPC功能有持久的,性别特异性的影响.
- 后代的HSPC在调解母亲肥胖的代谢后果方面发挥着作用.
- 这些发现强调了在孕产妇肥胖和后代健康的背景下考虑性别的重要性.
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