Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610072, China.
Kolling Institute of Medical Research, University of Sydney, Sydney, NSW 2065, Australia.
Genes (Basel). 2021 Oct 20;12(11):1653. doi: 10.3390/genes12111653.
Maternal obesity is a rapidly evolving universal epidemic leading to acute and long-term medical and obstetric health issues, including increased maternal risks of gestational diabetes, hypertension and pre-eclampsia, and the future risks for offspring's predisposition to metabolic diseases. Epigenetic modification, in particular DNA methylation, represents a mechanism whereby environmental effects impact on the phenotypic expression of human disease. Maternal obesity or overnutrition contributes to the alterations in DNA methylation during early life which, through fetal programming, can predispose the offspring to many metabolic and chronic diseases, such as non-alcoholic fatty liver disease, obesity, diabetes, and chronic kidney disease. This review aims to summarize findings from human and animal studies, which support the role of maternal obesity in fetal programing and the potential benefit of altering DNA methylation to limit maternal obesity related disease in the offspring.
母体肥胖是一种迅速演变的普遍流行疾病，导致急性和长期的医学和产科健康问题，包括增加母体患妊娠糖尿病、高血压和先兆子痫的风险，以及后代易患代谢疾病的未来风险。表观遗传修饰，特别是 DNA 甲基化，代表了一种环境影响影响人类疾病表型表达的机制。母体肥胖或营养过剩导致生命早期 DNA 甲基化的改变，通过胎儿编程，使后代易患许多代谢和慢性疾病，如非酒精性脂肪肝、肥胖、糖尿病和慢性肾脏病。本综述旨在总结支持母体肥胖在胎儿编程中的作用以及改变 DNA 甲基化以限制后代母体肥胖相关疾病的潜在益处的人类和动物研究的结果。
