Abstract
The review presents the results of experimental and clinical studies, according to which the absence of circadian melatonin production in pregnant women associated with the pathologies they have (obesity, diabetes mellitus, metabolic syndrome, pregnancy complicated by gestosis and chronic placental insufficiency, etc.) disrupts the genetic process of organizing the rhythmic activity of genes of the suprachiasmatic nuclei of the hypothalamus and melatonin production in the pineal gland of the fetus, leading to dysregulation of metabolic processes in the childs body after birth and programming pathology in following life. The significance of this factor in the pathophysiological mechanisms of catch-up growth during the first months of life determines a new approach to assessing the risk of obesity and necessitates learning the consequences of impaired development of the brain and other functional systems in fetuses that are born earlier than the 26th week of pregnancy and are thereby deprived of maternal melatonin, a key signaling molecule that directs and coordinates the genetic development process, during the most critical period of early ontogenesis.
Highlights
■■ В обзоре представлены результаты экспериментальных и клинических исследований, показавших, что отсутствие циркадианной продукции мелатонина у беременной, связанное с имеющейся у нее патологией, не только приводит к задержке становления ритмической активности специфических генов плода, но и лежит в основе дерегуляции метаболических процессов в организме ребенка и программирования патологии в последующие годы жизни
■■ The review presents the results of experimental and clinical studies, according to which the absence of circadian melatonin production in pregnant women associated with the pathologies they have disrupts the genetic process of organizing the rhythmic activity of genes of the suprachiasmatic nuclei of the hypothalamus and melatonin production in the pineal gland of the fetus, leading to dysregulation of metabolic processes in the child’s body after birth and programming pathology in following life
The significance of this factor in the pathophysiological mechanisms of catch-up growth during the first months of life determines a new approach to assessing the risk of obesity and necessitates learning the consequences of impaired development of the brain and other functional systems in fetuses that are born earlier than the 26th week of pregnancy and are thereby deprived of maternal melatonin, a key signaling molecule that directs and coordinates the genetic development process, during the most critical period of early ontogenesis
Summary
■■ В обзоре представлены результаты экспериментальных и клинических исследований, показавших, что отсутствие циркадианной продукции мелатонина у беременной, связанное с имеющейся у нее патологией (ожирение, сахарный диабет, метаболический синдром, гестоз, хроническая плацентарная недостаточность и т. п.), не только приводит к задержке становления ритмической активности специфических генов плода, но и лежит в основе дерегуляции метаболических процессов в организме ребенка и программирования патологии в последующие годы жизни. Роль отсутствия циркадного ритма материнского мелатонина в генезе раннего скачка роста у детей // Журнал акушерства и женских болезней.
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