Fetal diabetes in rats and its effect on placental glycogen

• Published in: Diabetologia 1985-04, Vol.28 (4), p.244-249
• Main Authors: BARASH, V, GUTMAN, A, SHAFRIR, E
• Format: Article
• Language: English
• Subjects: Animals; Biological and medical sciences; Diabetes Mellitus, Experimental - metabolism; Diseases of mother, fetus and pregnancy; Female; Glucose - metabolism; Glycogen - analysis; Glycogen - metabolism; Glycogen Synthase - metabolism; Gynecology. Andrology. Obstetrics; Insulin - metabolism; Insulin - pharmacology; Insulin - physiology; Liver Glycogen - metabolism; Medical sciences; Organ Size - drug effects; Pancreas - metabolism; Phosphorylases - metabolism; Placenta - metabolism; Pregnancy; Pregnancy. Fetus. Placenta; Rats
• ISSN: 0012-186X; 1432-0428
• DOI: 10.1007/BF00282241

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.