It has been previously shown that up to one third of women with a history of GDM develop the metabolic syndrome in a period of approximately ten years [6, 7]. The present study reveals that a number of metabolic risks such an unfavourable lipid profile, HOMA-IR and higher blood pressure were clustering at three months postpartum in women with GDM and that in women with GDM requiring insulin, the unfavourable metabolic profile was accompanied by significantly higher AASI than in the control women and in women with GDM controlled by nutritional therapy. Overall, at least three interesting conclusions can be drawn from this study. First, in women with GDM controlled by diet, the subtle increase in arterial stiffness observed during pregnancy was found to be totally reversible, although in the postpartum period they did not adhere to the prudent diet to which they were committed during pregnancy. This was reflected by the fact that the lipid profiles during pregnancy, but not postpartum, were similar or even somewhat better in the GDM than in the control group and accordingly the weight gain during, but not after pregnancy, was similar in both groups. Second, those women with GDM receiving insulin appeared to develop more severe dyslipidemia and exhibited an increasing trend in arterial stiffness after delivery, indicating that the metabolic disease in a stepwise manner was accompanied by notable changes in a vascular function and suggesting that there really was a dose and response type of relationship. Savvidou et al. have shown that pregnancies complicated by insulin resistance are associated with systemic maternal arterial stiffness increasing progressively from controls to gestational to type 2 diabetics which our results now confirm. The study of Davenport et al.  indicated that the vascular function of women in the early postpartum period is directly influenced by the development of GDM during pregnancy and by the persistence of clinical and/or subclinical hyperglycemia after delivery, a phenomenon observed also in our study.
AASI during pregnancy correlated positively with the mother’s age and the correlation with age and AASI after delivery was also almost statistically significant. These findings are in line with the results of previous studies . Pre-pregnancy BMI correlated also with AASI during pregnancy. Accordingly, the positive correlations with the night-time blood pressure values and the observed negative correlation with nocturnal diastolic dipping are phenomena that have been detected also in previous studies, confirming the validity of the present results .
A reduction in the decline in the nocturnal blood pressure is claimed to be a predictor for cardiovascular risk [21–23] and it also has been shown to be associated with arterial stiffness . This was also seen within the groups in the present study, even though the differences between the groups were not statistically significant.
The mechanisms behind the present results remain speculative, but they may be related to fundamentally different metabolism in women with metabolic risks. In the women with GDM, those with the lowest beta-cell function will require insulin in pregnancy  and the effect of providing insulin may have had some impact on the results i.e. insulin is known to possess vasodilatory properties and it may thus mask the effect of impaired glucose tolerance . On the other hand, the second half of pregnancy is known to be characterized by acquired insulin resistance that improves immediately after pregnancy. Furthermore, there is also a link between fat mass, lactation, sex steroids and glucose metabolism. We do not have any data on how many of the mothers in our study were breast-feeding, but three months after delivery, the vast majority, up to 78%, of mothers is known to breast-feed in Finland . Lactation is an oestrogen-deficient state, predisposing women to abdominal and visceral fat accumulation. The effect of oestrogen may be reflected in eating or activity behaviours and thus on mechanisms that have a direct effect also on glucose metabolism. Oestrogen treatment in mice is known to increase lipolysis in abdominal fat cells and to modulate leptin responsiveness in several ways. . Oestrogen deficiency in female animals is also known to be associated with hyperphagia and increased body weight, the effects probably being mediated by neuropeptide Y, agouti-related peptide, proopiomelancortin and ghrelin [34, 35]. However, little is known about the effects of lactation on vascular function, although the metabolic effects seen in the present study were clear-cut across the full spectrum of gestational glucose intolerance.
Impaired glucose tolerance and hypertensive problems during pregnancy have been considered to be a potential window into a woman’s future  revealing tendencies about whether she will suffer cardiovascular problems such as hypertension or diabetes mellitus later in life. In our study, there was transient stiffening in the arteries during pregnancy with a restoration of elasticity after delivery in the group of GDM women who were being controlled by nutritional treatment but not in the insulin requiring group, despite the fact that they adhered to a strict diet. Using the previously established cut-offs [15, 16], the AASI values were within the normal age-related limits in both groups and therefore, the clinical significance of the observed AASI changes will require further study. Overall, this may have true clinical significance, as it is believed that AASI predicts cardiovascular complications, even in normotensive subjects.
One weakness of our study was the rather small number of participants and in addition there quite many dropped out. One obvious reason for the considerable number of drop-outs was the presence of the newborn baby, who occupied all the mother’s attention. The optimal time for recording AASI values during pregnancy is not known. On the other hand, there is evidence that arterial elastic properties may worsen during the third trimester in normal pregnancies [37, 38], suggesting that AASI measurements would have been different if they had been conducted earlier in the pregnancy. In the current setting, third-trimester pregnant women were enrolled since pregnancy specific changes, such as GDM, had become manifested and were being diagnosed by that time. Accordingly, the normality of the controls could not have been verified earlier than near term, since many obstetric complications only appear in the third trimester. Otherwise, the subjects of the present study were young and were considered to be healthy before and after their pregnancy. The cut-off values for GDM diagnostics in OGTT in Finland have changed since our study, being now 5.3 -10-8.6 mmol/l, and there is the possibility that the results would have been changed slightly if the updated cut-off values had been used.