**1. Introduction**

Pregnancy is a very complex period where growth, development and maturity take place. The future body, in addition to increasing its cellular mass, progressively acquires functional capabilities that would permit it to live and grow out of the mother's womb [1, 2]. Two clear periods can be distinguished during pregnancy in the future mother. During the first period, a marked increase in insulin level and sensitivity occurs in the mother, with parallel increases in placenta size, amniotic volume, protein content and fat stores; however, the foetus weight gain is small in comparison with that of the mother [1–3]. During the second period, a physiological increase in insulin resistance and insulin degradation takes place in the mother, in parallel to the exponential foetal growth that partially or totally blocks the gain rhythm of maternal stores. This metabolic situation assures the availability of glucose for the maternal and foetal brains and mammary gland, reducing the uptake of glucose by other maternal tissues [1–3]. When glucose homeostasis is not physiologically balanced, changes and adaptation take place during pregnancy, predisposing the individual to degenerative diseases later in life [4–8]. In some non-diabetic women, an alteration in carbohydrate metabolism occurs during pregnancy; thus, although fasting glycaemia is normal, after a carbohydrate load, the glycaemia increases over normal values. This situation is rather more frequent at the end of pregnancy and is known as gestational diabetes (GD) [1, 9].

Several homeorhetic adjustments are required to assure adequate foetal anabolism, which in turn can also be affected by genetic and nutritional factors [1, 2, 10–15]. Maternal glucocorticoids, among others, clearly affect metabolites and foetal corticoids that compete with other anabolic and growth mediators as insulin and insulin-like growth factor-1 (IGF-1) [2, 16–18]. Thus, a hormonal balance seems to be of critical importance to guarantee suitable foetal and postnatal development [4, 5, 16–19]. Glucocorticoids are central hormones engaged in correct foetal growth and maturation [16, 17]; however, their excess induces intrauterine growth delay, clearly affecting glucose homeostasis and brain development and functions [20–22]. As discussed above, palliative mechanisms are available to reduce the negative effects of excess active corticoids [20–22].
