<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>Placental transfer of lactate, glucose and 2-deoxyglucose
was examined employing the <italic>in situ</italic> perfused
placenta. Control and streptozotocin induced diabetic
Wistar rats were infused with [U<sup>14</sup>C]-glucose and
[<sup>3</sup>H]-2-deoxyglucose (2DG). The fetal side of the placenta
was perfuseci with a cell free medium and glucose
uptake was calculated in the adjacent fetuses.
Despite the 5-fold higher maternal plasma glucose
concentration in the diabetic dams the calculated
fetal glucose metabolic index was not significantly
different between the 2 groups. Placental blood flow
was reduced in the diabetic animals compared with
controls but reduction of transfer of [U<sup>14</sup>C]-glucose and [<sup>3</sup>H]-2-deoxyglucose and endogenously derived
[<sup>14</sup>C]-Lactate to the fetal compartment, could not be
accounted for by reduced placental blood flow
alone. There was no significant net production or
uptake of lactate into the perfusion medium that
had perfused the fetal side of the placenta in either
group. The plasma lactate levels in the fetuses adjacent
to the perfused placenta were found to be higher
than in the maternal plasma and significantly
higher in the fetuses of the diabetic group compared
with control group. In this model the <italic>in situ</italic> perfused
placenta does not secrete significant quantities
of lactate into the fetal compartment in either
the control or diabetic group.</p>
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Int J Exp Diabetes Res. 2001; 2(2):113-120