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

Abstract

After 20 min infusion of L-IU- 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 I 14C)alanine and I 14C)lactate, with a minor percentage of I 1 4 C)glucose. Radioactivity in fetal plasma was much lower when the mothers were infused with aaminol 14C)isobutyric acid. The simultaneous infusion of aminooxyacetate decreased materno-fetal transfer of radioactivity from I 14C)alanine but not from a-amino! 14C)isobutyric acid, and this effect corresponded to a complete disappearance of the I 14 CJ lactate in fetal plasma without affecting I 14 CJ alanine levels or alanine concentration in the fetuses. Placenta slices in vitro metabolized L-IU- 14C)alanine into I 1 4 C)lactate and 14 CO2 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 a-aminol 14C)isobutyric acid was half that of IU- 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 a-amino! 14C)isobutyric acid as compared to that from I 1 4 C)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.