Abstract
Gestational diabetes mellitus (GDM) is a pregnancy complication first detected in the second or third trimester in women that did not show evident glucose intolerance or diabetes before gestation. In 2019, the International Diabetes Federation reported that 15.8% of live births were affected by hyperglycemia during pregnancy, of which 83.6% were due to gestational diabetes mellitus, 8.5% were due to diabetes first detected in pregnancy, and 7.9% were due to diabetes detected before pregnancy. GDM increases the susceptibility to developing chronic diseases for both the mother and the baby later in life. Under GDM conditions, the intrauterine environment becomes hyperglycemic, while also showing high concentrations of fatty acids and proinflammatory cytokines, producing morphological, structural, and molecular modifications in the placenta, affecting its function; these alterations may predispose the baby to disease in adult life. Molecular alterations include epigenetic mechanisms such as DNA and RNA methylation, chromatin remodeling, histone modifications, and expression of noncoding RNAs (ncRNAs). The placenta is a unique organ that originates only in pregnancy, and its main function is communication between the mother and the fetus, ensuring healthy development. Thus, this review provides up-to-date information regarding two of the best-documented (epigenetic) mechanisms (DNA methylation and miRNA expression) altered in the human placenta under GDM conditions, as well as potential implications for the offspring.
Highlights
Gestational diabetes mellitus (GDM) is a worldwide health concern affecting pregnant women and their offspring
The Diabetes Atlas published in 2019 by the International Diabetes Federation [1] reported that 15.8% of live births in 2019 were affected by hyperglycemia during pregnancy, of which 83.6% were due to gestational diabetes mellitus, 8.5% were due to diabetes first detected in pregnancy, and 7.9% were due to diabetes detected before pregnancy, increasing the susceptibility to developing chronic diseases in their adult life [2]
The authors observed a different miRNA exosome profile in the GDM group, with nine upregulated and 14 downregulated miRNAs, targeting signaling pathways associated with PI3K/Akt and mitogen-activated protein kinase (MAPK)/ERK1/2, both involved in cell proliferation [88,90]
Summary
Gestational diabetes mellitus (GDM) is a worldwide health concern affecting pregnant women and their offspring. The newborn affectations include macrosomia, hyperinsulinemia, and hypoglycemia [6] They become susceptible to developing cardiovascular diseases [9], obesity [10], type II diabetes [11], and metabolic disorders [12] in adulthood. Some theories have been proposed to explain how an individual could acquire these epigenetic marks, including (1) direct exposure to the environment throughout life, (2) events occurring during gestation affecting the fetus, and (3) transgenerational inheritance from the parental germline [17]. These modifications are not permanent but could persist for generations [18] as observed in plants and animal models. GDM can trigger epigenetic alterations in the placenta [22], such as DNA methylation variations [23], and misexpression of noncoding RNAs, of which the best studied are miRNAs [24]; these epigenetic mechanisms modulate gene expression and placental function
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