There is evidence that an abnormal intrauterine environment has consequence
s for later life. Intrauterine growth retardation is associated with low in
sulin secretion during fetal life and probably a reduced development of ins
ulin receptors. In later life these alterations can induce insulin resistan
ce. Macrosomia is associated with an increased insulin secretion during fet
al life and exhaustion of the insulin producing B cells. In later life a re
duced insulin secretion is found.
The working mechanisms have been explored in experimental studies. Normalis
ation of the diabetic intrauterine milieu can prevent consequences in later
life. There are also indications that vascular changes in later life can b
e reduced by anti-oxidantia.
In the human intrauterine growth retardation is related in later life with
insulin resistance, vascular diseases and preeclampsia; macrosomia is relat
ed with gestational diabetes and breastcarcinoma.