Glucose is one of the main nutrients for fetal development. Nevertheless, a
significant gluconeogenesis ability by the fetus has not been reported, therefore
the fetal glucose homeostasis depends on the ability of the placenta to carry out
glucose from the maternal blood and to transport it to fetal tissues by means of
specific transport molecules, known as GLUTs.
Several conditions contribute to an imbalance in fetal glucose homeostasis,
including incorrect mother feeding, maternal obesity, maternal type II diabetes
and/or pregnancy complications. These conditions can affect the normal
development of the fetus by affecting glucose transfer through the placenta.
Nowadays it is known that environmental contaminants are able to impair
placental glucose homeostasis compromising fetal development. These
substances include synthetic chemicals with estrogen-like behavior referred as to
Endocrine Disrupting Chemicals (EDCs), of which Bisphenol A represents one of
the most important for its wide distribution in many daily-use products.
However, in which way these two possible maternal perturbations (altered
glucose supply and BPA exposure) are able to interfere with placental glucose
uptake and how this interference may reflect on an incorrect fetal development
has to be elucidated. For this purpose, this study aimed to clarify the effect of
such perturbations on human placental glucose homeostasis.
The studies were conducted in vitro, in human placental cell line, and in vivo, in
rat placenta and fetal heart.
The results showed that both, altered glucose supply and BPA exposure, influence
human and rat placental glucose transport. Moreover, the in vivo study revealed
that BPA disruption on placental glucose homeostasis compromise fetal rat heart
development