Offspring of diabetics are at increased risk for diabetes as adults. As cor
ticosteroids are intimately involved in glucose homeostasis, we investigate
d aspects of corticosteroid activity in the late gestation fetuses of contr
ol, moderately diabetic and insulin-controlled streptozotocin-induced diabe
tic rats. We found that moderate maternal diabetes had no effect upon litte
r size or fetal body weight. Uncontrolled maternal diabetes was accompanied
by fetal hyperglycemia, hyperinsulinemia and elevated aldosterone. Materna
l insulin treatment normalized fetal glucose and aldosterone; fetal insulin
and corticosterone levels increased. Maternal diabetes had no effect upon
fetal adrenal expression of P450scc mRNA; the abundance of P450c11 beta mRN
A increased, and returned to that of the control gestation upon insulin tre
atment. P450c11AS mRNA was barely detectable, and decreased in the fetuses
of insulin-treated diabetics. P450c11B3 mRNA was undetectable in all fetal
groups. Our results implicate aspects of maternal diabetes in the expressio
n of a fetal adrenocortical imprint, manifested as a greater abundance of P
450c11 beta mRNA. Although not accompanied by elevated corticosterone in th
e fetus, this imprint could ultimately allow for greater potential corticos
terone production in response to typical stimuli, and thus contribute to th
e tendency towards glucose dysregulation in these offspring of diabetic ges
tations.