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Maternal and Placental DNA Methylation Changes Associated with the Pathogenesis of Gestational Diabetes Mellitus

Journal

NUTRIENTS
Volume 15, Issue 1, Pages -

Publisher

MDPI
DOI: 10.3390/nu15010070

Keywords

gestational diabetes mellitus (GDM); DNA methylation; epigenetics; insulin-like growth factor; adipokines; leptin; adiponectin; TNF-alpha; insulin resistance

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Gestational diabetes mellitus (GDM) is a significant metabolic complication of pregnancy that affects the future health of both the mother and the newborn. The pathogenesis of GDM is not fully understood, but it is clear that placental secretion of insulin-like growth factors, adipokines, tumor necrosis factor-alpha, cytokines, and insulin resistance play a key role. Additionally, DNA methylation of related molecules and pathway-related genes influence gene expression and contribute to the pathogenesis of GDM.
Gestational diabetes mellitus (GDM) is an important metabolic complication of pregnancy, which affects the future health of both the mother and the newborn. The pathogenesis of GDM is not completely clear, but what is clear is that with the development and growth of the placenta, GDM onset and blood glucose is difficult to control, while gestational diabetes patients' blood glucose drops and reaches normal after placenta delivery. This may be associated with placental secretion of insulin-like growth factor, adipokines, tumor necrosis factor-alpha, cytokines and insulin resistance. Therefore, endocrine secretion of placenta plays a key role in the pathogenesis of GDM. The influence of DNA methylation of these molecules and pathway-related genes on gene expression is also closely related to the pathogenesis of GDM. Here, this review attempts to clarify the pathogenesis of GDM and the related maternal and placental DNA methylation changes and how they affect metabolic pathways.

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