作为对母亲肥胖的反应,骨髓髓髓细胞的代谢和转录重塑
bioRxiv : the preprint server for biology
|September 4, 2024
概括
母亲肥胖会改变后代的骨髓脂质代谢和免疫基因表达,增加成人心脏代谢疾病的风险. 脂质配置和细胞功能的这些早期变化可能会导致长期的健康问题.
科学领域:
- 代谢研究研究 代谢研究
- 发展生物学 发展生物学
- 免疫学 免疫学 免疫学
背景情况:
- 孕产妇的肥胖是后代肥胖和心脏代谢疾病的重要危险因素.
- 之前的研究表明,肥胖母亲的后代在骨髓中发生了代谢和免疫障碍.
研究的目的:
- 为了研究肥胖母亲的后代骨髓脂质代谢的变化.
- 识别可能使后代易患成人发病的早期分子变化.
主要方法:
- 使用一种小鼠模型,研究母亲高脂肪饮食 (HFD) 诱导的肥胖症.
- 在骨髓细胞和从后代分离的髓状细胞上进行了脂质组,代谢组和转录组分析.
- 将高度养母亲 (Off-HFD) 的后代与常规养母亲 (Off-RD) 的后代进行比较.
主要成果:
- 非HFD后代在骨髓细胞中表现出二甲基甘油 (DAG),三甲基甘油 (TAG),脂,脂和脂的显著差异.
- 胆固醇乙水平下降,以及年龄相关的线粒体功能障碍.
- 观察到氨基酸和能量代谢的性别依赖性变化,以及骨髓状细胞中免疫基因表达的改变.
结论:
- 早期暴露于孕产妇肥胖导致后代骨髓细胞,特别是髓状细胞的深度脂质,代谢和转录变化.
- 这些分子变化可能是生命后期对代谢和心血管疾病易感性增加的基础.
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