Aims/hypothesis. To investigate the outgrowth of the ectoplacental cone in
diabetic rats in vivo and in vitro.
Methods. Female Wistar rats were injected intraperitoneally with streptozot
ocin (75 mg/kg body weight, n = 15), or with control buffer (n = 27) 3 days
before mating. On day 9 (day 1 = copulation plug) decidual swellings were
weighed and the volume and mitotic index of the embryo and ectoplacental co
ne were estimated. Also, ectoplacental cones were cultured either in the pr
esence of decidual cells from pseudopregnant diabetic rats or in high gluco
se concentration media. Cultures were evaluated by the daily outgrowth and
by the proportion of giant cells and proliferating cells on day 5.
Results. In diabetic rats on day 9, the weight of the decidual swellings an
d the mitotic index in the ectoplacental cone were lower compared with cont
rols (p < 0.0001 and p < 0.05, respectively). In vitro, control ectoplacent
al cones in the presence of decidual cells from diabetic rats showed a slig
ht reduction in outgrowth on day 3 and 5 of culture. Outgrowth of diabetic
ectoplacental cones in high glucose concentration medium was impaired on da
y 1 (p < 0.0005) compared with control ectoplacental cones in control mediu
m, and on day 1 and 2 (both p < 0.005) compared with control ectoplacental
cones in high glucose concentration medium. In control medium, the outgrowt
h of diabetic ectoplacental cones was impaired on day 1 (p < 0.05), compare
d with control ectoplacental cones. Proliferation was stimulated in diabeti
c ectoplacental cone cultures.
Conclusion/interpretation. These data suggest that the outgrowth of diabeti
c ectoplacental cones is impaired by high glucose concentrations.