Abstract
With the rising global tide of obesity, gestational diabetes mellitus (GDM) burgeoned into one of the most common antenatal disorders worldwide. Macrosomic babies born to diabetic mothers are more likely to develop risk factors for cardiovascular disease (CVD) before they reach adulthood. Rodent studies in offspring born to hyperglycemic pregnancies show vascular dysfunction characterized by impaired nitric oxide (NO)-mediated vasodilation and increased production of contractile prostanoids by cyclooxygenase 2 (COX-2). Vascular dysfunction is a key pathogenic event in the progression of diabetes-related vascular disease, primarily attributable to glucotoxicity. Therefore, glucose-induced vascular injury may stem directly from the hyperglycemic intrauterine environment of GDM pregnancy, as evinced by studies showing endothelial activation and inflammation at birth or in childhood in offspring born to GDM mothers. This review discusses potential mechanisms by which intrauterine hyperglycemia programs dysfunction in the developing vasculature.
Highlights
Gestational diabetes mellitus (GDM) is defined as glucose intolerance resulting in hyperglycemia that is first discovered during pregnancy
There is a paucity of available data with respect to the relationship between GDM and vascular function in human offspring; there is some evidence to suggest that endothelial activation and aberrant extracellular matrix remodeling present shortly after birth in babies born to GDM pregnancies
Later life risk for cardiovascular disease (CVD) in offspring born to GDM pregnancies may stem from direct effects of the intrauterine metabolic milieu on the developing vasculature
Summary
Gestational diabetes mellitus (GDM) is defined as glucose intolerance resulting in hyperglycemia that is first discovered during pregnancy. GDM typically develops in the second trimester when maternal insulin secretion fails to compensate for the progressive loss of insulin sensitivity, which serves to meet the glucose requirements of the growing fetus This failure to maintain glycemic control in the pregnancy-induced state of insulin resistance is thought to unmask an underlying maternal predisposition. Circulating levels of pro-inflammatory cytokines have been shown to independently predict the onset of GDM [13], and increased cytokine expression in subcutaneous adipose tissue of GDM women has been reported [14] This pre-existing adipose tissue dysfunction and low-grade inflammation are thought to underlie the amplification of pregnancy-induced maternal immune activation observed in GDM women. GDM arises when the physiological stress of pregnancy unmasks a maternal predisposition that stems from a complex interaction between genetic and environmental factors
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