Both pregestational [1] and gestational diabetes mellitus [2,3] can lead to neonatal macrosomia which is associated with fetal death, prematurity, birth trauma, and neonatal respiratory distress syndrome, hypoglycaemia, polycythaemia, hyperbilirubinaemia, hypocalcaemia, hypomagnesaemia and cardiomyopathy [4±6]. For macrosomic neonates, birth weight has not been consistently shown to positively correlate with the degree of control of maternal blood glucose [7,8], suggesting that factors other than or in addition to maternal blood glucose are associated with adverse clinical outcomes during diabetes in pregnancy.Offspring from pregnant women with diabetes are more likely to develop diabetes mellitus and obesity later in life. This observation and evidence that development of diabetes is more closely related to maternal than paternal health, suggests that the intrauterine environment is possibly of importance [9, 10]. Abstract Aims/hypothesis. Gestational diabetes is associated with complications for the offspring before, during and after delivery. Poor maternal glucose control, however, is a weak predictor of these complications. Given its position at the interface of the maternal and fetal circulations, the placenta possibly plays a crucial part in protecting the fetus from adverse effects from the maternal diabetic milieu. We hypothesised that gestational diabetes may result in changes in placental function, particularly with respect to the uptake, transfer, and/or utilisation of glucose. We aimed to examine glucose transport and utilisation in intact human placental lobules from women with gestational diabetes and those from normal pregnancies. Method. Dual perfusion of an isolated placental lobule was done on placentae from diet treated gestational diabetic (n = 7) and normal pregnant patients (n = 9) using maternal glucose concentrations of 4, 8,

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The aim of this study was to compare glucose transport and utilization in human placentae from pregnancies affected by insulin-treated GDM with and without macrosomia, and from non-diabetic control pregnancies. Placental lobules were perfused for 4 h. Maternal D-glucose concentration was 4, 8, 16, or 24 mM while the fetal D-glucose was maintained at 3mM. 14C-D-glucose and 3H-L-glucose were infused into the maternal circulation. Radioactivity, D-glucose and L-lactate levels were measured in the fetal and maternal effluent perfusates. Glucose uptake from the maternal perfusate, and transfer to the fetal effluent were not significantly different between groups. Insulin-treated GDM group without macrosomia had reduced glucose utilization compared to the control group while the insulin-treated GDM group with macrosomia did not. Lactate release into the fetal effluent was significantly reduced in both insulin-treated GDM groups compared to the control group. In conclusion, placental glucose utilization is different between insulin-treated GDM placentae with and without fetal macrosomia.