孕产妇的高血压疾病会改变后代的脂肪组织功能和血压敏感度
Ren Ozawa1, Hisataka Iwata1, Takehito Kuwayama1
1Laboratory of Animal Reproduction, Department of Animal Science, Tokyo University of Agriculture, 1737 Funako, Atsugi, Kanagawa, 234-0034, Japan.
Biochemical and biophysical research communications
|March 23, 2024
概括
怀孕期间由血管素II (Ang II) 诱导的孕产妇高血压导致胎盘功能障碍和胎儿生长限制. 后代表现出改变的脂质代谢和高血压,表明长期的健康影响.
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.
- 心血管生理学心血管生理学
背景情况:
- 孕前 (PE) 涉及母亲的高血压,并可能影响胎儿的发育.
- 在高血压条件下的子宫内环境可能会影响后代的健康.
- 脂质代谢和血压调节对于长期健康至关重要.
研究的目的:
- 研究孕产妇高血压对男性后代生长的影响,重点关注脂质代谢和血压.
- 确定安吉奥素II (Ang II) 诱导的母乳高血压如何影响小鼠的胎盘功能和胎儿发育.
- 评估这种子宫内环境对后代脂肪细胞功能和心血管健康的长期影响.
主要方法:
- 在雌性小鼠中诱导母性高血压,使用从妊娠12日开始的血管素II (Ang II) 输注.
- 对胎盘脂质失调和胎儿生长限制的分析.
- 评估出生体重和后代的体重变化.
- 在新生儿和成年后代的脂肪细胞中评估Pparγ mRNA表达.
- 在成年后代中测量基础血压和对高血压刺激的敏感性.
主要成果:
- Ang II诱导的孕产妇高血压导致胎盘脂质失调和胎儿生长限制,导致后代出生体重较低.
- 来自高血压母的新生儿和成年后代在脂肪组织中表现出更高的Pparγ mRNA表达.
- 成人后代在脂肪组织中增加了中性粒细胞和炎症单细胞.
- 与对照组相比,Ang II后代表现出较高的基础血压和对高血压刺激的敏感性增加.
- 虽然最初更轻,但Ang II后代的体重在16周后赶上了对照组.
结论:
- 由Ang II诱导的孕产妇高血压会破坏胎盘功能,导致胎儿生长受限和降低出生体重.
- 改变的子宫内环境会影响后代的脂肪细胞功能,其特征是增加Pparγ表达和炎症.
- 暴露于母亲高血压的后代表现出长期的心血管影响,包括血压升高和对高血压挑战的敏感性增加.
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