葡萄皮质类药物和非酒精性脂肪肝疾病的子宫内编程
Ze Chen1, Li-Ping Xia2, Lang Shen2
1Department of Pharmacology, Wuhan University School of Basic Medical Sciences, Wuhan 430071, China; Department of Cardiology, Zhongnan Hospital of Wuhan University, Wuhan 430072, China.
Metabolism: clinical and experimental
|November 1, 2023
概括
非酒精性脂肪肝 (NAFLD) 起源于子宫,通常是由于产前压力. 孕产妇的葡萄糖皮质类药物可以调节胎儿的肝脏代谢,增加后代的NAFLD风险.
科学领域:
- 生殖生物学 生殖生物学
- 发展规划是指发展规划.
- 代谢性疾病是一种代谢性疾病.
背景情况:
- 不酒精性脂肪肝 (NAFLD) 越来越多地被认为起源于胎儿发育期间.
- 不良的产前状况,如母亲营养不良或异生菌暴露,增加胎儿对NAFLD的敏感性.
- 葡萄糖皮质类药物在发育规划中发挥着关键作用,影响胎儿对疾病的易感性.
研究的目的:
- 审查流行病学和实验证据,将子宫内因子与NAFLD联系起来.
- 阐明NAFLD子宫内编程的机制,重点关注葡萄糖皮质激素暴露.
- 讨论胎儿起源的NAFLD的潜在生命早期干预措施.
主要方法:
- 对NAFLD和产前暴露的流行病学研究的审查.
- 对胎儿肝脏代谢的葡萄糖皮质激素编程实验证据的分析.
- 检查葡萄糖皮质体-胰岛素类生长因子1 (GC-IGF1) 轴的作用.
主要成果:
- 不良的子宫内环境导致过度暴露于母体的葡萄糖皮质激素,在表观遗传上改变胎儿的肝脂代谢.
- GC-IGF1轴的编程有助于产后生长障碍和代谢失调.
- 产后环境不匹配加剧了被编程的代谢变化,加速了NAFLD的发病.
结论:
- NAFLD具有明确的子宫内起源,通过葡萄糖皮质激素介导的发育编程来确定.
- 产前葡萄糖皮质激素过量引起的表观遗传修饰是关键机制.
- 针对生命早期的干预措施可能提供一种预防胎儿起源NAFLD的策略.
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