在生命早期通过调节 kynurenine 途径对肥胖的表观遗传编程
Mojgan Gharipour1, Jeffrey M Craig2,3, Garth Stephenson2
1School of Medicine, Faculty of Health at Deakin University, Melbourne, VIC, Australia. m.gharipour@deakin.edu.au.
International journal of obesity (2005)
|October 18, 2024
概括
怀孕期间的孕产妇炎症可能会通过通过表观遗传变化改变胎儿基因表达来增加儿童肥胖风险. 针对母亲炎症的干预措施可能会降低这种风险.
科学领域:
- 发育生物学是发展生物学.
- 免疫学 免疫学 免疫学
- 公共卫生 公共卫生
背景情况:
- 儿童肥胖是一个全球性的健康问题,其起源可能在出生前.
- 健康和疾病的发育起源 (DOHaD) 假设将子宫内环境与长期健康结果联系起来.
- 怀孕期间的母亲因素可以影响后代的免疫功能和疾病易感性.
研究的目的:
- 审查母亲炎症对儿童肥胖风险的影响.
- 探索表观遗传修饰和代谢途径在这种关系中的作用.
- 提出针对孕产妇炎症的潜在干预策略.
主要方法:
- 对有关母亲炎症,表观遗传学和儿童肥胖现有文献的综述.
- 检查金氨酸 (Kyn) 途径作为潜在的媒介.
- 假设Kyn途径代谢物在怀孕期间免疫调节中的作用.
主要成果:
- 怀孕期间母亲的炎症可能导致关键基因的表观遗传修饰.
- 这些修改可以影响代谢和信号通路,包括 kynurenine (Kyn) 途径.
- 基努瑞宁途径代谢物可能具有影响胎儿发育的免疫调节性质.
结论:
- 孕产妇的炎症是儿童肥胖的一个重要危险因素,由表观遗传变化介导.
- kynurenine (Kyn) 途径及其代谢物与调节妊娠炎症和后代风险有关.
- 改善孕产妇炎症状况的干预措施可能是减轻儿童肥胖风险的策略.
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