Abstract
Gestational Diabetes Mellitus (GDM) is defined as glucose intolerance that develops in the second or third trimester of pregnancy. GDM can lead to short-term and long-term complications both in the mother and in the offspring. Diagnosing and treating this condition is therefore of great importance to avoid poor pregnancy outcomes. There is increasing interest in finding new markers with potential diagnostic, prognostic and therapeutic utility in GDM. Non-coding RNAs (ncRNAs), including microRNAs, long non-coding RNAs and circular RNAs, are critically involved in metabolic processes and their dysregulated expression has been reported in several pathological contexts. The aberrant expression of several circulating or placenta-related ncRNAs has been linked to insulin resistance and β-cell dysfunction, the key pathophysiological features of GDM. Furthermore, significant associations between altered ncRNA profiles and GDM-related complications, such as macrosomia or trophoblast dysfunction, have been observed. Remarkably, the deregulation of ncRNAs, which might be linked to a detrimental intrauterine environment, can lead to changes in the expression of target genes in the offspring, possibly contributing to the development of long-term GDM-related complications, such as metabolic and cardiovascular diseases. In this review, all the recent findings on ncRNAs and GDM are summarized, particularly focusing on the molecular aspects and the pathophysiological implications of this complex relationship.
Highlights
Introduction and GDM OverviewGestational Diabetes Mellitus (GDM) is a metabolic disease diagnosed in the second or third trimester of pregnancy [1]
The inhibition of miR-101 decreases enhancer of zester homolog 2 (EZH2) levels in GDM-human umbilical vein endothelial cells (HUVECs) and the silencing of EZH2 in GDM-HUVECs or the overexpression of EZH2- β in healthy HUVECs induced the increase in miR-101 expression. These results indicate a reciprocal regulation of miR-101 and EZH2 in HUVECs and suggest that the imbalance observed in GDM might be responsible for the higher expression of miR-101 and the functional alterations of endothelial cells, such as decreased survival and functional capacity [125]
GDM diagnosis is generally performed in the late second trimester, when the metabolic alterations have already developed and emerge at the oral glucose tolerance test (OGTT)
Summary
Gestational Diabetes Mellitus (GDM) is a metabolic disease diagnosed in the second or third trimester of pregnancy [1]. The identification of phenotypic classes associated with adverse outcomes, defined by the presence of some risk factors, turned out to be potentially useful in customizing and modulating the diagnostic and therapeutic approach in GDM [16,17]. Preventing and treating this condition likely contributes to limiting the burden of the disease. As regards β-cell dysfunction, it has been observed that β-cell function is reduced by 30–70% in GDM, indicating that β-cells are unable to compensate for the increase in insulin resistance, resulting in the development of GDM [28]. The understanding of their functions might help unravel the complex pathophysiological mechanisms in GDM and contextually identify novel potential diagnostic biomarkers for the disease
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