Through complex hormonal pathways, insulin resistance can lead to the activation of the sympathetic nervous system, and vice versa. Schobel et al. showed that in PE patients, mus-cle sympathetic nerve activity (MSNA) is increased compared with normotensive pregnant and non-pregnant women. Studies assessing heart-rate variability and plasma noradrenalin concentrations also suggest increased sympathetic activity in PE. It has been hypothesized that sympathetic over-activity is a precursor of PE, normally compensated for by vasodilating mechanisms, but resulting in PE when the mechanisms fail. In addition to sympathetic activity, various markers of inflamma-tion are also associated with reduced insulin sensitivity, suggesting that chronic sub-clinical inflamma-tion could be part of the insulin resistance syndrome. The role of sympathetic over-activity and inflammatory markers in gestational diabetes has not been investigated