The pathophysiology of gestational diabetes mellitus (GDM) remains unclear. Current consensus indicates that women with GDM have a greater degree of insulin resistance, cell dysfunction, central obesity and hyperlipidaemia, which would imply that GDM is a transient manifestation of an underlying state of metabolic dysfunction. Hyperglycaemia is acknowledged as the principal factor responsible for the complications of DMT2 but, together with oxidative stress, it can also play an important role in GDM and the development of mother-foetus complications. The relationships between GDM and oxidative stress and the importance of the oxidant/antioxidant balance are not clearly understood. Some studies have shown associations between GDM and markers of oxidative stress; an increase in oxidative stress and a decrease in anti-oxidative defence in GDM have been observed. These data suggest that oxidative stress can be implicated in the progression and/or pathogenesis of GDM, and that the reduced antioxidant defences can reflect a protective response to an existing oxidative stress. Markers of oxidative stress and inducible nitric oxide synthase (iNOS) have been described as being overexpressed in GDM placenta, which could be related to cell damage. GDM placenta may be pre-conditioned by transient intracellular oxidative stress to attenuate the responsiveness to further oxidative insult. However, the effects of oxidative as well as nitrosative stress in GDM placenta, and the impact that they could have on perinatal morbidity and risk of future complications, need to be elucidated. This review centres on the importance of oxidative/nitrosative stress in the pathophysiology of GDM and their effects in GDM placenta. The relevance of equilibrium between inductor and protector mechanisms in metabolic control, obstetric complications, and perinatal outcomes are reviewed.
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