glycogen and Fetal-Resorption

The placenta provides all energy and nutrient requirements for healthy fetal development. The placenta in rats is capable of storing glycogen, although the placenta cells must therefore mobilize stored glycogen to its own glucose supply. Moreover, maternal glucose and/or placental lactate furnished the fetal growth. Adult female Wistar rats were divided into three groups: Control-C, tumour bearing-W; injected ascitic fluid-A. The rats were sacrificed on the 16th, 19th or 21st day of gestation, analysing the placenta and fetus weights and placental tissue samples was aliquoted for biochemical assays of glycogen and protein content and alkaline phosphatase activity. Placental sections were morphometrically analysed and glycogen positive cells were counted. The placental and fetal weight were significantly reduced in both W and A rats from 16th up to 21st day of gestation, which showed high levels of fetal reabsorption sites. Significant reduction in labyrinth zone at day 21 in both tumour bearing and ascitic fluid injected groups was shown, suggesting less substrate exchange at the maternal/fetal surface. The alkaline phosphatase activity as well total protein content were found to be reduced in W and A group. The total placental glycogen and glycogen cells decreased during tumour bearing and ascitic fluid injection, suggesting reduction in its own stored energy. Ascitic fluid injected group, representing an indirect tumour effect, presented similar reduction changes in the placenta to the tumour-bearing group. In conclusion, the tumour growth and, especially, ascitic fluid injection promoted irreversible placental tissue damage altering homeostasis and compromising fetal development.

Topics: Alkaline Phosphatase; Animals; Carcinoma 256, Walker; Cell Count; Decidua; Female; Fetal Resorption; Fetal Weight; Glycogen; Organ Size; Placenta; Pregnancy; Rats; Rats, Wistar; Trophoblasts

Topics: Animals; Body Weight; Female; Fetal Resorption; Glycogen; Organ Size; Pregnancy; Pregnancy, Animal; Proteins; Pseudopregnancy; Rats; Rats, Inbred Strains; Rotenone; Uterus

An acute dose (10 mg/100 g body weight) of biotin at the post-implantation stage (day 14 and 15) inhibited the fetal and placental growth, and in few rats it also caused resorption of fetuses and placentae. The maintenance of pregnancy with normal fetal and placental growth was effected with estrogen therapy, but progesterone failed to correct the biotin-induced effect. The uterine and placental glycogen, RNA and protein levels, as well as, glucose-6-phosphate dehydrogenase activity in the ovary, liver and uterus showed a reduction following biotin treatment. Estrogen therapy under such conditions corrected these adverse effects of biotin overdose, while progesterone had no significant effects. The study suggests that the acute dose of biotin at an advance stage of pregnancy may cause adverse effects on the physiological regulation of gestation, possibly by creating deficiency of estrogen and gestagen. The possible role of estrogen in the fetal and placental growth and regulation of gestagen secretion is discussed.

Topics: Animals; Biotin; Embryonic Development; Estradiol; Female; Fetal Resorption; Glucosephosphate Dehydrogenase; Glycogen; Gonadal Steroid Hormones; Nucleic Acids; Organ Size; Placenta Diseases; Pregnancy; Pregnancy Complications; Pregnancy, Animal; Progesterone; Rats; Reproduction