Stresses during pregnancy that increase maternal
glucocorticoids reduce
birth weight in several species. However, the role of natural
glucocorticoids in the mother in fetal acquisition of nutrients for growth remains unknown. This study aimed to determine whether fetal growth was reduced as a consequence of altered
amino acid supply when mice were given
corticosterone in their
drinking water for 5 day periods in mid to late pregnancy (day, D, 11-16 or D14-19). Compared to controls drinking tap water,
fetal weight was always reduced by
corticosterone. At D16,
corticosterone had no effect on materno-fetal transfer of [(14)C]methylaminoisobutyric
acid (
MeAIB), although placental
MeAIB accumulation and expression of the Slc38a1 and Slc38a2 transporters were increased. However, at D19, 3 days
after treatment ended, materno-fetal transfer of
MeAIB was increased by 37% (P < 0.04). During treatment at D19, placental accumulation and materno-fetal transfer of
MeAIB were reduced by 40% (P < 0.01), although expression of Slc38a1 was again elevated. Permanent reductions in placental vascularity occurred during the earlier but not the later period of treatment. Placental Hsd11b2 expression, which regulates feto-placental
glucocorticoid bioavailability, was also affected by treatment at D19 only. Maternal
corticosterone concentrations inversely correlated with materno-fetal
MeAIB clearance and
fetal weight at D19 but not D16. On D19,
weight gain of the maternal carcass was normal during
corticosterone treatment but reduced in those mice treated from D11 to D16, in which
corticosterone levels were lowest. Maternal
corticosterone is, therefore, a physiological regulator of the
amino acid supply for fetal growth via actions on placental phenotype.