Maternal Melatonin Deficiency Leads to Endocrine Pathologies in Children in Early Ontogenesis

Int J Mol Sci. 2021 Feb 19;22(4):2058. doi: 10.3390/ijms22042058.

Abstract

The review summarizes the results of experimental and clinical studies aimed at elucidating the causes and pathophysiological mechanisms of the development of endocrine pathology in children. The modern data on the role of epigenetic influences in the early ontogenesis of unfavorable factors that violate the patterns of the formation of regulatory mechanisms during periods of critical development of fetal organs and systems and contribute to the delayed development of pathological conditions are considered. The mechanisms of the participation of melatonin in the regulation of metabolic processes and the key role of maternal melatonin in the formation of the circadian system of regulation in the fetus and in the protection of the genetic program of its morphofunctional development during pregnancy complications are presented. Melatonin, by controlling DNA methylation and histone modification, prevents changes in gene expression that are directly related to the programming of endocrine pathology in offspring. Deficiency and absence of the circadian rhythm of maternal melatonin underlies violations of the genetic program for the development of hormonal and metabolic regulatory mechanisms of the functional systems of the child, which determines the programming and implementation of endocrine pathology in early ontogenesis, contributing to its development in later life. The significance of this factor in the pathophysiological mechanisms of endocrine disorders determines a new approach to risk assessment and timely prevention of offspring diseases even at the stage of family planning.

Keywords: children; early ontogenesis; endocrine pathology; family planning; melatonin.

Publication types

  • Review

MeSH terms

  • Child
  • Circadian Rhythm / physiology
  • Endocrine System / physiology*
  • Female
  • Fetal Development
  • Fetus / physiology
  • Humans
  • Melatonin / deficiency*
  • Metabolic Networks and Pathways
  • Pregnancy

Substances

  • Melatonin