Aims/hypothesis. Gestational diabetes is associated with complications for
the offspring before, during and after delivery. Poor maternal glucose cont
rol, however is a weak predictor of these complications. Given its position
at the interface of the maternal and fetal circulations, the placenta poss
ibly plays a crucial part in protecting the fetus from adverse effects from
the maternal diabetic milieu. We hypothesised that gestational diabetes ma
y result in changes in placental function, particularly with respect to the
uptake, transfer, and/or utilisation of glucose. We aimed to examine gluco
se transport and utilisation in intact human placental lobules from women w
ith gestational diabetes and those from normal pregnancies.
Method. Dual perfusion of an isolated placental lobule nas done on placenta
e from diet treated gestational diabetic (n = 7) and normal pregnant patien
ts (n = 9) using maternal glucose concentrations of 4, 8, 16 and 24 mmol/l
in random order over a 4-h experiment. Results were expressed in mu mol . m
in(-1) . g(-1).
Results. D-glucose uptake from the maternal circulation (control 0.492 vs g
estational diabetes mellitus 0.248, at 8 mmol/l maternal glucose), D-glucos
e utilisation by the placenta (0.255 vs 0.129), D-glucose transfer to the f
etal circulation (direct 0.979 vs 0.402; net transfer 0.269 vs 0.118) and L
-lactate maternal release into both the fetal (0.052 vs 0.042) and maternal
(0.255 vs 0.129) circulation were significantly reduced during in vitro pe
rfusion of placentae from patients with gestational diabetic pregnancies. T
ransfer of H-3-L-glucose also significantly reduced in the diabetic group (
8.1 % vs 2.6 %).
Conclusion/interpretation. These results suggest that placental transport a
nd metabolism of D-glucose is altered during gestational diabetes.