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.
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http://dx.doi.org/10.3390/ijms22042058 | DOI Listing |
J Anim Sci
December 2024
Department of Animal and Dairy Sciences, Mississippi State University, Mississippi State, MS, 39762, USA.
The neuroendocrine hormone melatonin is associated with circadian rhythms and has antioxidant and vasodilative properties. In cattle, melatonin rescues fetal growth during maternal nutrient restriction in a seasonally dependent manner, but melatonin research in swine is limited. The objective of this study was to evaluate effects of dietary melatonin supplementation during mid to late gestation on circadian rhythm and muscle growth and development of the longissimus dorsi in utero and postnatally.
View Article and Find Full Text PDFBreastfeed Med
December 2024
Australian Centre for Behavioural Research in Diabetes, Deakin University, Melbourne, Victoria, Australia.
Tryptophan is an essential amino acid that is not produced in the body and can only be consumed through diet. Tryptophan is a precursor for serotonin, which, in turn, helps produce melatonin. Melatonin exhibits a circadian rhythm, peaking at night and dissipating during the day, with basal levels significantly differing between mothers.
View Article and Find Full Text PDFJ Pineal Res
November 2024
Laboratory of Developmental Chronobiology, Instituto de Anatomía, Histología y Patología, Facultad de Medicina, Universidad Austral de Chile, Valdivia, Chile.
Gestational chronodisruption, increasingly common due to irregular light exposure, disrupts maternal-fetal circadian signaling, leading to long-term health issues in offspring. We utilized a chronic photoperiod shifting model (CPS) in pregnant rats to induce chronodisruption and investigated the potential mitigating effects of maternal melatonin supplementation (CPS + Mel). Male and female offspring were evaluated at 3 ages (90, 200, and 400 days of age) for metabolic profiles, hormonal responses, cytokine levels, and adipose tissue activity.
View Article and Find Full Text PDFElife
December 2024
College of Life Sciences, Institute of Reproductive Sciences, Key Laboratory of Animal Reproduction and Germplasm Enhancement in Universities of Shandong, Qingdao Agricultural University, Qingdao, China.
Maternal obesity has deleterious effects on the process of establishing oocyte DNA methylation; yet the underlying mechanisms remain unclear. Here, we found that maternal obesity disrupted the genomic methylation of oocytes using a high-fat diet (HFD) induced mouse model, at least a part of which was transmitted to the F2 oocytes and livers via females. We further examined the metabolome of serum and found that the serum concentration of melatonin was reduced.
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