Glycogen content in the normal placenta decreases gradually towards term. However, in human diabetes and in rat
streptozotocin diabetes two- to tenfold increases in placental
glycogen level were found during the pregnancy. This elevation was evident in rats per tissue weight,
protein or
DNA content and was also seen in
insulin-treated and gestational diabetics. Electron microscopic investigation of diabetic rat placenta revealed
glycogen deposition in the typical
glycogen cells, also in junctional zone cells and in all cells of the placental labyrinth. Placental
glycogen accumulation in diabetes occurs in marked contrast to other tissues, such as maternal liver, from which
glycogen disappears. Liver and muscle glycogenesis and glycogenolysis are under
insulin control, by regulation of the activities of
glycogen synthase and
phosphorylase. However, in the placenta these
enzymes are not meaningfully influenced by
insulin in in vivo and in vitro studies. In our and other laboratories the activities of both
enzymes somewhat increased or decreased, showing no trend conducive to
glycogen accumulation. Placenta is
glucose dependent, but the role of
insulin in its carbohydrate metabolism is doubtful. Despite the high placental concentration of
insulin receptors no metabolic outcome has yet been pointed out.
Glycogen accumulation in the placenta of diabetic rats was found to be related to the extent of maternal
hyperglycemia. The resultant markedly increased intracellular level of
glucose-6-phosphate accelerates
glycogen synthesis b.
Glucose itself activates
glycogen synthase and deactivates
glycogen phosphorylase. Continuous
glucose infusion to non-diabetic pregnant rats on gestation days 18-21 likewise also caused an increase in placental
glycogen in correlation with
hyperglycemia. The possibility that placental
glycogen is under the control of fetal rather than maternal
insulin was explored by producing
insulin deficiency through intrafetal
streptozotocin injection. There was no effect of fetal "diabetes" on placental
glycogen synthesis or on the distribution of placental
glycogen between the maternal and fetal segments of the placenta, while it caused a marked decrease in the fetal
liver glycogen content and
fetal body weight. To assess the availability of placental
glycogen as an energy source the placental glycogenolysis was investigated after hormonal stimulation.
Catecholamines were effective in inducing
lactate formation both in vivo and in vitro in nondiabetic and diabetic rats. Protracted activation of the
adenylate cyclase system by
cholera toxin administration pronouncedly reduced placental
glycogen in vivo.