Placental formation of lactate from transferred L-alanine and its impairment by aminooxyacetate in the late-pregnant rat.

After 20 min infusion of L-[U-14C]alanine through the left uterine artery in 21-day-pregnant rats, the radioactivity in the plasma of fetuses from the left uterine horn was much higher than in their mothers and was composed of approximately equal parts of [14C]alanine and [14C]lactate, with a minor percentage of [14C]glucose. Radioactivity in fetal plasma was much lower when the mothers were infused with alpha-amino[14C]isobutyric acid. The simultaneous infusion of aminooxyacetate decreased materno-fetal transfer of radioactivity from [14C]alanine but not from alpha-amino[14C]isobutyric acid, and this effect corresponded to a complete disappearance of the [14C]lactate in fetal plasma without affecting [14C]alanine levels or alanine concentration in the fetuses. Placenta slices in vitro metabolized L-[U-14C]alanine into [14C]lactate and 14CO2 at the rate of 7 nmol/g per min, and this process was inhibited by the presence of 1 mM aminooxyacetate in the medium. Placental uptake of alpha-amino[14C]isobutyric acid was half that of [U-14C]alanine, and aminooxyacetate did not affect this parameter with either of the labelled compounds. Results indicate that the lower transfer to the rat fetus of the 14C atoms from alpha-amino[14C]isobutyric acid as compared to that from [14C]alanine is due not only to the diminished placental carrier system of the former but also to its non-metabolyzable condition. It is proposed that the capacity of the placenta to metabolyze L-alanine to lactate and the subsequent release of lactate to the fetus constitute important factors for the fetal metabolic economy.