Adverse neonatal outcomes continue to be high for mothers with type 1 and type 2 diabetes, and are far from eliminated in mothers with gestational diabetes mellitus. This is often despite seemingly satisfactory glycaemic control in the latter half of pregnancy. Here we argue that this could be a consequence of the early establishment of fetal hyperinsulinaemia, a driver that exaggerates the fetal glucose steal. Essentially, fetal hyperinsulinaemia, through its effect on lowering fetal glycaemia, will increase the glucose concentration gradient across the placenta and consequently the glucose flux to the fetus. While the steepness of this gradient and glucose flux will be greatest at times when maternal hyperglycaemia and fetal hyperinsulinaemia coexist, fetal hyperinsulinaemia will favour a persistently high glucose flux even at times when maternal blood glucose is normal. The obvious implication is that glycaemic control needs to be optimised very early in pregnancy to prevent the establishment of fetal hyperinsulinaemia, further supporting the need for pre-pregnancy planning and early establishment of maternal glycaemic control. An exaggerated glucose steal by a hyperinsulinaemic fetus could also attenuate maternal glucose levels during an OGTT, providing an explanation for why some mothers with fetuses with all the characteristics of diabetic fetopathy have 'normal' glucose tolerance.
Keywords: Diabetic fetopathy; Fetal glucose steal; Fetal hyperinsulinaemia; Gestational diabetes mellitus; Placenta; Pregnancy; Review; Transplacental glucose transfer; Type 1 diabetes; Type 2 diabetes.