The role of fetal
insulin in placental
glycogen accumulation, which occurs despite
insulin deficiency in maternal diabetes, was studied in rats.
Streptozotocin was injected into fetuses of non-diabetic and
streptozotocin-diabetic mothers on days 19.5 and 20.5 of gestation, causing fetal hypoinsulinaemia and pancreatic
insulin depletion. Placental
glycogen content of either 1.6 mg/g in non-diabetic rats or 6.5 mg/g in diabetic rats was not affected by fetal
streptozotocin treatment.
Glycogen distribution was also measured in the placenta to assess the effect of fetal hypoinsulinaemia on
glycogen content in its fetal segment. The
glycogen concentration ratio between the fetal and maternal segments in diabetic rats was approximately 0.3 and increased to approximately 0.5 in diabetic rats, without being affected by fetal hypoinsulinaemia. There was no significant effect of fetal hypoinsulinaemia on the activities of placental
glycogen synthase or
glycogen phosphorylase, both in non-diabetic and diabetic rats. Fetal hypoinsulinaemia was associated, however, with a marked decrease in fetal
liver glycogen together with a decrease in fetal liver weight, which was more pronounced than the decrease in
fetal body weight. Administration of
insulin to the
streptozotocin-treated fetuses restored the impaired
glycogen synthesis (measured by incorporation of U-[14C]-
glucose and 3H2O in the fetal liver) without affecting
glycogen synthesis in the placenta.(ABSTRACT TRUNCATED AT 250 WORDS)