Abstract
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 the 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.
Highlights
Specialty section: This article was submitted to Obesity, a section of the journal Frontiers in Endocrinology
In adipocytes differentiated from mesenchymal stem cells (MSCs) in Wharton’s jelly of umbilical cord tissue of small for gestational age (SGA) neonates, it was reported that the increased acyl-coenzyme A synthetase 1 (ACSL1) was highly associated with histone acetylation and could be a programmable mediator of insulin sensitivity and cellular lipid content [164]
Fetal epigenetic programming is a concept that the intrauterine environment induced fetal epigenetic modification and associated gene expression activity is relatively stably transmitted after birth until adults, and thereby decide the physiological phenotype in adult from fetal development
Summary
Reviewed by: Karen Vrijens, University of Hasselt, Belgium Sean L. Fetal metabolic programming caused by the adverse intrauterine environment can induce metabolic syndrome in adult offspring. 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. It is proposed that an adverse intrauterine environment can induce fetal metabolic programming of obesity and insulin resistance and further metabolic syndrome in adult offspring. Epigenetic programming, without DNA nucleotide sequence changes, is a critical underlying mechanism of fetal metabolic programming of metabolic syndrome in adult offspring [2,3,4,5,6].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
