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Epigenetic Programming and Fetal Metabolic Programming.

Ziqiang Zhu1,2, Fang Cao2, Xiaozhong Li1

  • 1Children's Hospital of Soochow University, Suzhou, China.

Frontiers in Endocrinology
|December 19, 2019
PubMed
Summary
This summary is machine-generated.

Adverse intrauterine environments can cause fetal metabolic programming, leading to adult metabolic syndrome. Epigenetic programming is a key mechanism, altering gene expression without changing DNA sequence.

Keywords:
adverse intrauterine environmentepigenetic programmingfetal metabolic programminginsulin resistancemetabolic syndromeobesity

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Area of Science:

  • Developmental biology
  • Metabolic disorders
  • Epigenetics

Background:

  • Adverse intrauterine environments can lead to fetal metabolic programming.
  • This programming can result in metabolic syndrome, including obesity and insulin resistance, in adult offspring.
  • The precise mechanisms underlying fetal metabolic programming are not fully understood.

Purpose of the Study:

  • To provide an overview of the critical role of epigenetic programming in fetal metabolic programming.
  • To explore how epigenetic modifications contribute to metabolic syndrome development.
  • To highlight the link between intrauterine environment and long-term metabolic health.

Main Methods:

  • Review of existing literature on fetal metabolic programming.
  • Analysis of studies investigating epigenetic mechanisms.
  • Synthesis of evidence linking intrauterine environment, epigenetics, and metabolic syndrome.

Main Results:

  • Epigenetic programming is a critical underlying mechanism of fetal metabolic programming.
  • Adverse intrauterine environments induce epigenetic modifications affecting gene expression and cellular function.
  • These modifications can be stably retained and transmitted, contributing to metabolic syndrome.

Conclusions:

  • Epigenetic programming plays a vital role in fetal metabolic programming.
  • Understanding these epigenetic changes is crucial for addressing metabolic syndrome.
  • Interventions targeting the intrauterine environment may mitigate long-term metabolic risks.