Epigenetic programming and fetal metabolic programming
- 1Children's Hospital of Suzhou University, China
- 2Changzhou Maternal and Child Health Care Hospital, China
Fetal metabolic programming caused by the adverse intrauterine environment can induce metabolic syndrome in adult offspring. Adverse intrauterine environment introduces fetal long-term relatively irreversible changes in organs and metabolism, and thus causes fetal metabolic programming leading metabolic syndrome in adult offspring. Fetal metabolic programming of obesity and insulin resistance plays a key role in this process. The mechanism of fetal metabolic programming is still not very clear. It is suggested that epigenetic programming, also induced by adverse intrauterine environment, is a critical underlying mechanism of fetal metabolic programming. Fetal epigenetic programming affects gene expression changes and cellular function through epigenetic modifications without DNA nucleotide sequence changes. Epigenetic modifications can be relatively stably retained and transmitted through mitosis and generations, and thereby induce the development of metabolic syndrome in adult offspring. This manuscript provides an overview of the critical role of epigenetic programming in fetal metabolic programming.
Keywords: epigenetic programming, Fetal metabolic programming, Adverse intrauterine environment, metabolic syndrome, Insulin Resistance, Obesity
Received: 03 Sep 2018;
Accepted: 21 Oct 2019.
Copyright: © 2019 Zhu, Cao and Li. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Prof. Xiaozhong Li, Children's Hospital of Suzhou University, Suzhou, China, XiaoxiaoLi_cn@163.com