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

International journal of molecular sciences
January 1, 1970
Dmitry O Ivanov et al. (6 authors)
Journal ArticleReviewHuman Study
Study Details

Study Goal

The researchers aimed to determine the role of melatonin in regulating metabolic processes and its protective effects on fetal development, particularly in preventing endocrine pathology.

Results Summary

The study found that melatonin plays a key role in regulating fetal circadian rhythms and protecting genetic programs during pregnancy complications. Maternal melatonin deficiency disrupts hormonal and metabolic regulation in offspring, increasing the risk of endocrine disorders later in life.

Population

Children and fetuses, particularly in the context of maternal melatonin levels during pregnancy.

Effective Dosage

Not specified

Duration

Not specified

Interactions

None mentioned

Extracted Claims (8)
InterventionDirectionEndpointPopulationDosageImpactClaim #
melatonin
neutral
metabolic processes
-
-
participates in the regulation of metabolic processes
#1
maternal melatonin
neutral
circadian system of regulation
fetus
-
plays a key role in the formation of the circadian system of regulation
#2
maternal melatonin
neutral
genetic program of morphofunctional development
fetus
-
protects the genetic program of morphofunctional development
#3
melatonin
decrease
gene expression
-
-
prevents changes in gene expression
#4
melatonin
neutral
DNA methylation and histone modification
-
-
controls DNA methylation and histone modification
#5
deficiency and absence of the circadian rhythm of maternal melatonin
decrease
genetic program for the development of hormonal and metabolic regulatory mechanisms
child
-
underlies violations of the genetic program for the development of hormonal and metabolic regulatory mechanisms
#6
deficiency and absence of the circadian rhythm of maternal melatonin
increase
endocrine pathology
offspring
-
determines the programming and implementation of endocrine pathology
#7
deficiency and absence of the circadian rhythm of maternal melatonin
increase
endocrine pathology
offspring
-
contributes to its development in later life
#8
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.

Medical Subject Headings (MeSH)
ChildCircadian RhythmEndocrine SystemFemaleFetal DevelopmentFetusHumansMelatoninMetabolic Networks and PathwaysPregnancy
Study Links
Quality Scores
SafetyNot Assessed
Efficacy85/10
Quality75/10
Citation Metrics
Total Citations8
Citations/Year2.0
Relative Citation Ratio0.91
NIH Percentile46.8%
Research Impact Scores
APT Score0.25
Weight Score1.57
Normalized Score0.69
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